Module 9: 1.Patho: Define the factors influencing infection. Flashcards

1
Q

What are some factors that can cause damage to the human body?

A

Factors include sunlight, pollutants, physical trauma, infectious agents like viruses and bacteria, and internal factors like cancer.

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2
Q

How can damage impact the body?

A

Damage can range from affecting a single cell to multiple cells, tissues, or organs, potentially leading to disease and, in severe cases, death.

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3
Q

Why does the body need defense mechanisms?

A

The body requires defense mechanisms to protect against the various factors that can cause damage, ensuring its survival and well-being.

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4
Q

What is innate immunity?

A

Innate immunity, also called natural immunity, comprises physical and biochemical barriers and inflammation, which protect the body from injury and infection.

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5
Q

What is the role of physical and biochemical barriers in innate immunity?

A

These barriers are the first line of defense, present from birth, to prevent damage and thwart infections by harmful microorganisms. They can also host helpful microorganisms known as the “normal flora.”

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6
Q

What happens if an injurious agent breaches the surface barriers?

A

If an injurious agent penetrates the surface barriers, the second line of defense, the inflammatory response, is activated to protect the body from further injury, prevent infection, and promote healing.

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7
Q

Describe the nature of the inflammatory response.

A

The inflammatory response is a rapid and relatively nonspecific reaction to different types of tissue damage, initiated regardless of the specific cause. It aims to protect the body.

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8
Q

What is the third line of defense in the body’s immune system?

A

The third line of defense is adaptive (acquired) immunity, also known as specific immunity.

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9
Q

How does adaptive immunity differ from innate immunity in terms of speed and specificity?

A

Adaptive immunity is slower and more specific, targeting particular invading microorganisms.

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10
Q

What is the role of “memory” in adaptive immunity?

A

Memory in adaptive immunity results in a faster response upon re-exposure to the same microorganism.

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11
Q

What are the three levels of human defenses?

A

The three levels of human defenses are Barriers, Innate Immunity, and Adaptive (Acquired) Immunity.

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12
Q

What is the primary role of Barriers in the defense system?

A

Barriers serve as the first line of defense, providing physical and biochemical protections, including skin, mucous membranes, and secretory molecules.

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13
Q

What characterizes the second line of defense, Innate Immunity?

A

Innate Immunity represents the second line of defense and involves immediate responses like inflammation, along with cells such as mast cells, neutrophils, and macrophages.

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14
Q

How is Adaptive (Acquired) Immunity different from the other defense levels in terms of specificity?

A

While Barriers and Innate Immunity have broad specificity, Adaptive (Acquired) Immunity is highly specific, targeting specific antigens.

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15
Q

What is the role of memory in the immune system?

A

While Barriers and Innate Immunity have broad specificity, Adaptive (Acquired) Immunity is highly specific, targeting specific antigens.

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16
Q

What is the role of memory in the immune system?

A

Adaptive immunity involves specific immunological memory, allowing for a faster and more efficient response upon re-exposure to the same antigen.

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17
Q

Which cells are involved in the third line of defense, Adaptive Immunity?

A

T cells, B cells, macrophages, and dendritic cells are among the cells involved in Adaptive (Acquired) Immunity.

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18
Q

What are some active molecules used in human defenses?

A

Active molecules include defensins, complement, antibodies, and various cytokines.

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19
Q

How does each level of defense provide protection?

A

Barriers offer protection through physical and biochemical mechanisms, Innate Immunity uses inflammation and immune cells, while Adaptive (Acquired) Immunity employs activated T and B cells, antibodies, and cytokines for protection.

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20
Q

What are the external physical barriers in the body?

A

The external physical barriers consist of tightly associated epithelial cells in the skin and linings of the gastrointestinal, genitourinary, and respiratory tracts.

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21
Q

How does the body remove pathogens attempting to breach these barriers?

A

Mechanical processes like coughing, sneezing, vomiting, flushing by urine, and the continual replacement of dead epithelial cells remove pathogens.

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22
Q

What is the role of mucus and cilia in the upper respiratory tract?

A

Epithelial cells in the upper respiratory tract produce mucus and have hair-like cilia that trap and move pathogens upward, leading to their expulsion through coughing and sneezing.

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23
Q

How do low temperatures and low pH levels contribute to defense against microorganisms?

A

Low temperatures and low pH levels on the skin and in the stomach generally inhibit the growth of microorganisms, as most microorganisms require higher temperatures and near-neutral pH for efficient growth.

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24
Q

What protective substances are secreted by epithelial cells to guard against infection?

A

Epithelial cells secrete mucus, perspiration, saliva, tears, and earwax.

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25
Q

How do perspiration, tears, and saliva combat Gram-positive bacteria?

A

Perspiration, tears, and saliva contain lysozyme, an enzyme that attacks the cell walls of Gram-positive bacteria.

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26
Q

What substances are secreted by sebaceous glands in the skin, and what do they do?

A

Sebaceous glands secrete fatty acids and lactic acid, which have bactericidal properties against bacteria and fungi.

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27
Q

How does the pH environment created by glandular secretions affect bacteria?

A

Glandular secretions create an acidic and inhospitable environment with a pH range of 3 to 5, which is hostile to most bacteria.

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28
Q

What are antimicrobial peptides, and where are they found?

A

Antimicrobial peptides are small molecules that kill or inhibit the growth of disease-causing bacteria, fungi, and viruses. They are found in epithelial cell secretions.

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29
Q

How do cathelicidins work against bacteria, and where are they produced?

A

Cathelicidins disrupt bacteria by inserting into their cholesterol-free cell membranes. They are produced in epithelial cells of the skin, gut, urinary tract, and respiratory tract.

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30
Q

When is cathelicidin released, and by which cells?

A

Neutrophils, mast cells, and monocytes store cathelicidin and release it during inflammation.

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31
Q

What are the two subtypes of human defensins, and how do they differ in activation?

A

Human defensins come in two subtypes: α-defensins and β-defensins. α-defensins require activation by proteolytic enzymes, while β-defensins do not.

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32
Q

How do α-defensins work to combat bacteria, and where are they found?

A

α-defensins work with neutrophils to kill bacteria. They are also present in Paneth cells in the small intestine, protecting against disease-causing microorganisms.

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33
Q

Where are β-defensins primarily located, and what infections can they potentially guard against?

A

β-defensins are abundant in epithelial cells lining the respiratory, urinary, and intestinal tracts, as well as in the skin. They may help protect against infections like adenovirus (common cold) and human immunodeficiency virus (HIV).

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34
Q

What is the role of antimicrobial peptides in activating the body’s defense systems?

A

Both α-defensins and β-defensins can activate cells involved in subsequent levels of defense, including innate and acquired immunity.

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35
Q

What are collectins, and what do they do in the body?

A

Collectins are glycoproteins produced by the lung, including surfactant proteins A-D and mannose-binding lectin. They interact with carbohydrates on the surfaces of pathogenic microorganisms and aid macrophages in recognizing and eliminating these microorganisms.

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36
Q

How does mannose-binding lectin (MBL) contribute to immune defense?

A

MBL is adept at recognizing a common sugar on microorganism surfaces. It activates the complement plasma protein system, resulting in damage to bacteria or increased recognition by macrophages.

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37
Q

What is the normal microbiome, and where is it found in the body?

A

The normal microbiome consists of various microorganisms and is located on the body’s surfaces, including the skin, mucous membranes, GI tracts, respiratory tract, urethra, and vagina.

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38
Q

Do the microorganisms in the microbiome typically cause diseases?

A

No, the microorganisms in the microbiome do not typically cause diseases.

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39
Q

How would you describe the relationship between the microbiome and humans?

A

The relationship between the microbiome and humans can be commensal, where one benefits without affecting the other, or mutualistic, benefiting both.

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40
Q

What happens in the lower gut shortly after birth?

A

The lower gut is initially sterile at birth, but it quickly begins to get colonized by bacteria. The number, diversity, and concentration of these microorganisms increase progressively during the first year of life.

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41
Q

What are some of the benefits provided by the normal microbiome in the GI tract?

A

The benefits include the production of digestive enzymes, generation of essential metabolites like vitamins, and the release of antibacterial factors to prevent colonization by harmful microorganisms.

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42
Q

How do some members of the normal microbiome in the colon inhibit the growth of pathogenic microorganisms?

A

They produce toxic chemicals and proteins, compete for nutrients with pathogens, and block their attachment to the epithelium, a crucial step in the infection process.

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43
Q

How does the normal microbiome in the gut influence the adaptive immune system?

A

It promotes the growth of gut-associated lymphoid tissue, where most adaptive immune cells reside, and contributes to the development of both local and systemic adaptive immunity.

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44
Q

What is the role of GI bacteria in the brain-gut axis, and how does it impact various aspects of human health?

A

GI bacteria play a role in modulating cognitive function, behavior, pain, and stress responses through their influence on the brain-gut axis.

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45
Q

What can prolonged use of broad-spectrum antibiotics do to the normal microbiome?

A

Prolonged antibiotic use can disrupt the normal microbiome, reducing its protective activity and promoting overgrowth of harmful microorganisms.

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46
Q

What are some of the potential consequences of microbiome disruption in the intestine?

A

Disruption of the microbiome can lead to the overgrowth of Candida albicans and Clostridium difficile, potentially causing conditions like pseudomembranous colitis.

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47
Q

What is the role of Lactobacillus in the normal GI and vaginal microbiome of healthy women?

A

Lactobacillus produces protective chemicals like hydrogen peroxide, lactic acid, and bacteriocins, which help prevent infections in the vagina and urinary tract by other microorganisms.

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48
Q

How does prolonged antibiotic treatment affect Lactobacillus colonization and what are the associated risks?

A

Extended antibiotic use can reduce the presence of Lactobacillus, increasing the risk of urological or vaginal infections, such as vaginosis.

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49
Q

What types of microorganisms are predominantly found on the skin, and what variations exist?

A

Predominantly, the skin hosts Gram-positive cocci and rods. Specific areas may have variations, and some individuals may also carry yeasts like Candida and Pityrosporum.

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50
Q

What is the typical composition of microorganisms in the nose?

A

The nose primarily contains Gram-positive cocci and rods. Some individuals may carry pathogenic bacteria like S. aureus and β-hemolytic streptococci.

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51
Q

Describe the complex mix of bacteria found in the mouth.

A

The mouth hosts a complex mix of bacteria, including several species of streptococci, Actinomyces, lactobacilli, and Haemophilus. Anaerobic bacteria and spirochetes colonize gingival crevices.

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52
Q

What microorganisms are typically present in the colon?

A

The colon contains a diverse range of microorganisms, including Bacteroides, lactobacilli, clostridia, Salmonella, Shigella, Klebsiella, Proteus, Pseudomonas, enterococci, and other streptococci, bacilli, and Escherichia coli.

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53
Q

Which bacteria are typically found in the distal urethra, and what other microorganisms might be present?

A

The distal urethra typically contains bacteria found on the skin, such as S. epidermidis and diphtheroids. It may also have lactobacilli and nonpathogenic streptococci.

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54
Q

How does the composition of the vaginal microbiome change with age?

A

The vaginal microbiome varies with age. In newborns, it’s similar to adults. From 1 month to puberty, S. epidermidis, diphtheroids, E. coli, and streptococci are common. During puberty to menopause, Lactobacillus acidophilus becomes dominant. Postmenopause, it becomes similar to the prepubescent microbiome.

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55
Q

What is the primary purpose of the inflammatory response?

A

The inflammatory response is designed to limit tissue damage, eliminate infectious microorganisms, initiate adaptive immunity, and promote healing.

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56
Q

What are the four key characteristics of the inflammatory response?

A

The four key characteristics are: (1) it occurs in tissues with a blood supply, (2) it is activated rapidly (within seconds) after damage occurs, (3) it depends on both cellular and chemical components, and (4) it is nonspecific, responding similarly to various stimuli.

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57
Q

Why does inflammation occur in tissues with a blood supply?

A

Inflammation occurs in vascularized tissues because they have a blood supply, allowing for a rapid and efficient response to damage or infection.

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58
Q

How quickly does the inflammatory response become activated after tissue damage?

A

The inflammatory response is activated very rapidly, often within seconds after tissue damage occurs.

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59
Q

What is meant by the nonspecific nature of inflammation?

A

The nonspecific nature of inflammation means that it responds in a similar way regardless of the type of stimulus or whether exposure to the same stimulus has occurred in the past.

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60
Q

What can activate the inflammatory response in vascularized tissues?

A

Virtually any injury, including infection, tissue necrosis (e.g., ischemia, trauma, chemical injury), foreign bodies, and immune reactions, can activate the inflammatory response.

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61
Q

What are the cardinal signs of acute inflammation described by Celsus?

A

The cardinal signs are rubor (redness), calor (heat), tumour (swelling), dolor (pain), and functio laesa (loss of function).

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62
Q

What happens at the microscopic level near the site of injury during inflammation?

A

Microscopic changes include vasodilation (increased blood vessel size), increased vascular permeability with fluid leakage (edema), and white blood cell adherence and migration through vessel walls.

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63
Q

How does vasodilation contribute to inflammation?

A

Vasodilation leads to slower blood velocity and increased blood flow at the injury site, contributing to redness and warmth.

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64
Q

What causes the swelling (edema) associated with inflammation?

A

Increased vascular permeability and fluid leakage out of the vessels cause swelling (edema) at the site of injury.

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65
Q

What are the key components involved in inflammation at the site of injury?

A

Inflammation involves leukocytes (especially neutrophils), plasma proteins, and various biochemical mediators in the blood and tissues.

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66
Q

How do vascular changes contribute to inflammation?

A

Vascular changes allow the delivery of leukocytes, plasma proteins, and mediators to the injury site, promoting the inflammatory response.

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67
Q

What role do some chemical mediators play in inflammation?

A

Some chemical mediators activate pain fibers, contributing to the sensation of pain during inflammation.

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68
Q

How does tissue injury, pain, and swelling collectively affect the body?

A

Tissue injury, pain, and swelling can lead to a loss of function at the site of inflammation.

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69
Q

What happens to lymphatic vessels during inflammation, and what are the consequences for lymph nodes?

A

Lymphatic vessels drain extravascular fluid to lymph nodes. Inflammation can lead to lymphangitis in the lymph vessels and lymphadenitis in the nodes, which become hyperplastic, enlarged, and painful.

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70
Q

What are the benefits of inflammation in preventing infection and further damage?

A

Inflammation prevents infection by invading microorganisms, dilutes bacterial toxins, and activates plasma protein systems to contain and destroy bacteria. Phagocytes (neutrophils, macrophages) eliminate cellular debris and microorganisms.

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71
Q
A
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72
Q

How does inflammation limit and control the inflammatory process?

A

Inflammation prevents the spread of the inflammatory response to areas of healthy tissue through the influx of plasma protein systems, plasma enzymes, and cells (e.g., eosinophils).

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73
Q

How does inflammation interact with the adaptive immune system?

A

Inflammation brings macrophages and lymphocytes to the site, which destroy pathogens, eliciting a more specific immune response.

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74
Q

What is the role of inflammation in preparing the area of injury for healing and repair?

A

Inflammation removes bacterial products, dead cells, and other inflammatory substances, creating a favorable environment for healing and repair.

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75
Q

How does the drainage of fluid and debris at an inflamed site contribute to the development of acquired immunity?

A

Fluid and debris are drained by lymphatic vessels, allowing microbial antigens in lymphatic fluid to encounter lymphocytes in the lymph nodes, contributing to acquired immunity.

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76
Q

What are the three key plasma protein systems essential to an effective inflammatory response?

A

The three key plasma protein systems are the complement system, clotting system, and kinin system.

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77
Q

What is a common characteristic of these plasma protein systems in their inactive forms?

A

In their inactive forms, these systems comprise multiple proteins, with some being enzymes circulating as proenzymes.

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78
Q

How are the components within these systems activated during inflammation?

A

Activation of the initial components triggers sequential activation of other components, creating cascades, referred to as the complement cascade, clotting cascade, or kinin cascade.

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79
Q

What may be required for the activation of a specific protein in these systems?

A

In some cases, activation of a particular protein may require enzymatic cleavage into two differently sized fragments.

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80
Q

What are the three plasma protein systems involved in inflammation?

A

The three plasma protein systems are the Complement, Clotting, and Kinin systems.

81
Q

How is the complement system activated, and what are the major components produced during its activation?

A

The complement system can be activated by three mechanisms, leading to the proteolytic activation of C3. The major components produced are C3a and C3b.

82
Q

What are the functions of C3a and C3b in the complement system?

A

C3a acts as a potent anaphylatoxin that triggers mast cell degranulation, while C3b can bind to cell surfaces (e.g., bacteria) for phagocytosis and activate the next complement component, C5.

83
Q

How is the clotting system initiated, and what is the role of thrombin in this system?

A

The clotting system can be initiated by the tissue factor (extrinsic) or contact activation (intrinsic) pathways, leading to the activation of factor X and thrombin. Thrombin proteolytically activates fibrinogen to form fibrin, which promotes clot formation and increases vascular permeability.

84
Q

How is the kinin system linked to the clotting system, and what role does bradykinin play in inflammation?

A

XIIa produced by the clotting system can be activated by kallikrein from the kinin system. Kallikrein converts prekallikrein to kininogen, which activates bradykinin. Bradykinin increases vascular permeability, acts similarly to histamine, and stimulates pain through nerve endings.

85
Q

What percentage of the total circulating serum protein do the proteins of the complement system constitute?

A

The proteins of the complement system make up approximately 10% of the total circulating serum protein.

86
Q

What is the primary outcome of complement system activation in terms of immune defense?

A

Activation of the complement system results in the production of factors that can directly destroy pathogens or boost the activity of various components in the immune response.

87
Q

Which type of infection are the factors produced during complement system activation particularly effective against?

A

The factors produced during complement system activation are highly effective defenders against bacterial infections.

88
Q

What is the primary function of opsonins in the complement cascade?

A

Opsonins coat the surface of bacteria, increasing their susceptibility to being phagocytized and killed by inflammatory cells.

89
Q

What do chemotactic factors do in the context of inflammation?

A

Chemotactic factors diffuse from an inflammation site and attract phagocytic cells to that location.

90
Q

How do anaphylatoxins, such as C3a and C5a, contribute to inflammation?

A

Anaphylatoxins induce rapid degranulation of mast cells, leading to histamine release, vasodilation, and increased capillary permeability, which are essential components of inflammation.

91
Q

Which complement products are considered the most potent, and what are their roles?

A

The most potent complement products are C3b (opsonin), C3a (anaphylatoxin), and C5a (anaphylatoxin and chemotactic factor).

92
Q

What is the result of activating terminal complement components C5b through C9?

A

Activation of these components leads to the formation of a membrane attack complex (MAC), which creates pores in the outer membranes of cells or bacteria, causing cell death.

93
Q

What is the primary activator of the classical complement pathway?

A

Antibodies, which are components of the acquired immune system, serve as the primary activators of the classical pathway.

94
Q

What must happen before the classical complement pathway can be activated?

A

Antibodies need to bind to their targets, known as antigens, typically found on bacteria or other infectious agents.

95
Q

How does the classical pathway initiate complement activation?

A

Activation of the classical pathway begins with the first complement component, C1, and leads to the subsequent activation of complement components like C3 and C5.

96
Q

Which immune system component can use the classical pathway to combat bacteria and trigger inflammation?

A

Antibodies from the acquired immune response can use the classical pathway.

97
Q

How does the alternative complement pathway differ from the classical pathway in terms of activation?

A

The alternative pathway is activated by specific substances on the surface of infectious organisms directly, without the need for antibodies.

98
Q

How does the lectin pathway differ from the classical pathway in terms of activation?

A

The lectin pathway does not rely on antibodies for activation, while the classical pathway is antibody-dependent.

99
Q

What initiates the lectin pathway of complement activation?

A

he lectin pathway is initiated by several plasma proteins that recognize specific carbohydrate patterns on the surfaces of pathogenic microorganisms.

100
Q

What types of infectious agents can be targeted by the lectin pathway?

A

The lectin pathway can target a wide range of pathogenic microorganisms, including bacteria, viruses, protozoa, and fungi, based on the specific carbohydrate patterns they exhibit.

101
Q

Why is the lectin pathway important for complement activation?

A

The lectin pathway provides an additional means of complement activation, ensuring that even infectious agents unable to activate the complement system directly through the alternative pathway can still be targeted by complement.

102
Q

What are the four primary functions of complement cascade products?

A

The four functions of complement cascade products are opsonization (C3b), anaphylatoxic activity resulting in mast cell degranulation (C3a, C5a), leukocyte chemotaxis (C5a), and cell lysis (C5b–C9, also known as the membrane attack complex or MAC).

103
Q

What is the primary role of the clotting (coagulation) system?

A

The clotting system is responsible for forming blood clots in response to injuries to blood vessels.

104
Q

What does a blood clot consist of?

A

A blood clot is composed of a meshwork of protein strands, primarily fibrin. It also contains platelets and can trap other cells like erythrocytes, phagocytes, and microorganisms.

105
Q

What are the three primary functions of blood clots?

A

Blood clots serve three main functions: plugging damaged blood vessels to stop bleeding, trapping microorganisms to prevent their spread to nearby tissues, and providing a framework for future tissue repair and healing.

106
Q

What can activate the clotting system?

A

The clotting system can be activated by various substances released during tissue injury and infection, including collagen, proteinases, kallikrein, plasmin, and bacterial products such as endotoxins.

107
Q

How does the clotting system resemble the complement system?

A

imilar to the complement cascade, the clotting system can be activated by multiple pathways, ultimately leading to the formation of a blood clot.

108
Q

What is tissue factor (TF) and its role in the clotting system?

A

Tissue factor (TF), also known as tissue thromboplastin, is released by damaged endothelial cells in blood vessels. It activates the extrinsic pathway of the clotting system.

109
Q

How is the intrinsic pathway of the clotting system activated?

A

Damage to the vessel wall initiates the intrinsic (or contact activation) pathway, which involves contact between Hageman factor (factor XII) in plasma and negatively charged subendothelial substances.

110
Q

What is the common pathway activated by both the intrinsic and extrinsic pathways of the clotting system?

A

The common pathway leads to the activation of factor X, which, in turn, initiates the formation of fibrin to create a fibrin clot.

111
Q

How does activation of the clotting system contribute to the inflammatory response?

A

Activation of the clotting system produces protein fragments called fibrinopeptides (FPs) A and B, which have chemotactic effects on neutrophils and increase vascular permeability, enhancing the inflammatory response. Fibrinopeptide B works in synergy with bradykinin from the kinin system.

112
Q

What is the relationship between the kinin system and the coagulation system?

A

The kinin system interacts closely with the coagulation system, and the activation of Hageman factor (factor XII) to factor XIIa can initiate both systems.

113
Q

What is another name for factor XIIa, and what role does it play in the kinin system?

A

Factor XIIa is also known as prekallikrein, and it enzymatically activates the first component of the kinin system.

114
Q

What is the final product of the kinin system, and where does it come from?

A

The final product of the kinin system is bradykinin, which is derived from a larger precursor molecule called kininogen.

115
Q

What are the effects of bradykinin on the body?

A

Bradykinin causes the dilation of blood vessels, acts in conjunction with prostaglandins to induce pain, triggers the contraction of smooth muscle cells, and increases vascular permeability.

116
Q

Why is tight regulation of the interactions between the three plasma protein systems essential?

A

Tight regulation is crucial because these systems are highly interactive, and their activation can result in the production of potent biologically active substances. Regulation is necessary to ensure the efficient activation of the inflammatory process and to prevent potentially harmful effects on the individual.

117
Q

What are the two main reasons for the strict regulation of these plasma protein systems?

A

The first reason is that the inflammatory process is critical for an individual’s survival, and efficient activation must be guaranteed, regardless of the cause of tissue injury. The second reason is that the biochemical mediators generated during these processes are potent and potentially detrimental to the individual, and their action should be limited to only injured or infected tissues.

118
Q

What are some mechanisms to regulate plasma protein systems during inflammation?

A

Enzymes found in the plasma that enters tissues during inflammation, like carboxypeptidase, kininases, and histaminase, can inactivate mediators of inflammation.

119
Q

How is clot formation related to the regulation of these systems?

A

The formation of clots triggers the fibrinolytic system, which limits clot size and removes clots after bleeding stops. This helps regulate the plasma protein systems involved in inflammation.

120
Q

How does plasmin, formed during clot dissolution, interact with other cascades?

A

Plasmin can activate both the complement cascade (components C1, C3, and C5) and the kinin cascade by activating factor XII and producing prekallikrein activator.

121
Q

What is the role of C1 esterase inhibitor (C1 INH) in regulating inflammation?

A

C1 INH inhibits complement activation, helping to regulate the inflammatory response.

122
Q

What condition results from a genetic defect in C1 INH?

A

Hereditary angioedema, characterized by self-limiting edema of cutaneous and mucosal layers.

123
Q

How do some cells protect themselves from complement damage?

A

They have factors on their cell membrane surfaces that prevent the activation of C3 and inhibit the membrane attack complex (MAC) to protect against complement damage.

124
Q

What is inflammation, and where does it occur in the body?

A

Inflammation is a process that happens in both blood vessels and the surrounding tissues.

125
Q

What is the role of endothelial cells in blood vessels during inflammation?

A

Endothelial cells in blood vessels help regulate blood flow and also coordinate blood clotting and the movement of cells and fluid during inflammation.

126
Q

Name two types of cells found in tissues near blood vessels that are involved in the inflammatory response.

A

The two types of cells are mast cells, which activate inflammation, and dendritic cells, which connect the innate and acquired immune responses.

127
Q

What are the three main types of cells found in the blood?

A

The three main types of cells in the blood are erythrocytes (red blood cells), platelets, and leukocytes (white blood cells).

128
Q

What is the main function of erythrocytes in the blood?

A

Erythrocytes carry oxygen to the body’s tissues.

129
Q

How do platelets contribute to the blood’s function?

A

Platelets are involved in blood clotting, helping to stop bleeding.

130
Q

What are leukocytes, and how are they classified?

A

Leukocytes are white blood cells. They are classified into granulocytes, monocytes, and lymphocytes.

131
Q

What distinguishes granulocytes from each other, and what are the three main types of granulocytes?

A

Granulocytes differ based on the staining of their granules. The three main types of granulocytes are basophils, eosinophils, and neutrophils.

132
Q

What do monocytes eventually become, and where are they found in the body?

A

Monocytes mature into macrophages and are found in various tissues.

133
Q

What are the roles of lymphocytes in the immune system, and which lymphocytes are involved in the innate and acquired immune responses?

A

Lymphocytes have various immune system roles. Natural killer (NK) cells participate in the innate immune response, while B and T cells are involved in the acquired immune response.

134
Q

What is the role of immune system cells in response to molecules at the site of cellular damage?

A

Immune system cells respond to these molecules to enhance protective responses.

135
Q

Where do the molecules that trigger immune cell responses come from?

A

These molecules can originate from damaged cells, invading microbes, activation of plasma proteins, or secretions from other immune system cells.

136
Q

How do immune cells recognize these molecules, and what happens when they do?

A

Immune cells have specific surface receptors that bind to these molecules, leading to intracellular signaling and cell activation.

137
Q

What can happen when immune cells are activated in response to these molecules?

A

Immune cell activation can result in gaining functions important for the inflammatory response, releasing more substances that increase inflammation, or both.

138
Q

What are the primary goals of inflammatory cells and proteins at the site of tissue injury?

A

Inflammatory cells and proteins work to limit damage, combat microorganisms, clear cellular debris, and promote healing, tissue regeneration, or repair at the injury site.

139
Q

What are the surface receptors used by B and T lymphocytes in the adaptive immune system?

A

B and T lymphocytes use surface receptors known as BCR and TCR, respectively, to bind to a wide range of antigens.

140
Q

What type of receptors do cells in the innate immune system have, and what do these receptors recognize?

A

Cells in the innate immune system have pattern recognition receptors (PRRs) that recognize specific molecules or ligands.

141
Q

What are the two types of molecular patterns that PRRs can identify?

A

PRRs recognize pathogen-associated molecular patterns (PAMPs) found on infectious agents and damage-associated molecular patterns (DAMPs) from cellular damage.

142
Q

How does the recognition of PAMPs and DAMPs benefit the innate immune system?

A

Recognizing both PAMPs and DAMPs allows the innate immune system to respond to both sterile (DAMPs) and septic (PAMPs and DAMPs) tissue damage.

143
Q

Approximately how many different PRRs are there, and how many molecules can they recognize?

A

There are at least 100 different PRRs, each capable of recognizing over 1,000 different molecules.

144
Q

Where are PRRs generally found in the body, and what is their role?

A

PRRs are mainly present in surface tissues like the skin, respiratory tract, GI tract, and genitourinary tract. They monitor the environment for signs of cellular damage and potential infectious microorganisms.

145
Q

How do different classes of cellular PRRs differ from one another?

A

Different classes of cellular PRRs differ in the types of ligands they can bind.

146
Q

What are the different locations where PRRs can be found within the cell?

A

PRRs can exist on the cell surface, in endosomes (vesicles inside the cell), in the cytosol (inside the cell), or they can be secreted into the extracellular environment.

147
Q

Can you provide an example of a secreted PRR, and what pathway is it associated with?

A

Mannose-Binding Lectin (MBL) is an example of a secreted PRR, and it is associated with the lectin pathway of complement activation.

148
Q

What do Toll-like receptors (TLRs) primarily recognize?

A

TLRs primarily recognize pathogen-associated molecular patterns (PAMPs) on microorganisms.

149
Q

Where can PAMPs be located on microorganisms, and what are some examples of PAMPs?

A

PAMPs can be found on the cell wall, surface structures, and nucleic acids of microorganisms. Examples include bacterial lipopolysaccharide (LPS), peptidoglycans, bacterial flagellin, and viral double-stranded RNA.

150
Q

How many TLRs are known in humans?

A

There are 11 known TLRs in humans.

151
Q

Where are TLRs found on the surface of cells, and what types of cells have them?

A

TLRs are found on the surface of cells that have early contact with potential pathogens, including mucosal epithelial cells, mast cells, neutrophils, macrophages, dendritic cells, and some lymphocyte subpopulations.

152
Q

What pathways are activated by TLRs, and what do these pathways lead to?

A

TLRs activate pathways leading to the production of cytokines through NF-κB and antiviral type I interferons through interferon regulatory factors (IRFs).

153
Q

What types of cells have complement receptors, and what do these receptors recognize?

A

Complement receptors are found on various immune cells and some epithelial cells. They recognize specific fragments produced during complement system activation, such as C3a, C5a, and C3b.

154
Q

What is the primary role of scavenger receptors, and on which cells are they primarily found?

A

Scavenger receptors primarily facilitate the recognition and phagocytosis of bacterial pathogens, damaged cells, and altered lipoproteins associated with vascular damage. They are primarily found on macrophages.

155
Q

Can scavenger receptors recognize specific components of the cell membrane, and if so, what component?

A

Yes, some scavenger receptors, like SR-PSOX, can recognize the cell membrane component phosphatidylserine (PS). This is externalized during erythrocyte senescence and cellular apoptosis.

156
Q

Why is it important that scavenger receptors can recognize externalized phosphatidylserine?

A

Scavenger receptors recognizing phosphatidylserine help macrophages identify and remove old red blood cells and cells undergoing apoptosis.

157
Q

What are NOD-like receptors (NLRs), and where are they located?

A

NLRs are receptors found inside cells that can recognize substances from microbes and damaged cells.

158
Q

How many different NLRs are there in humans?

A

Humans have at least 22 different NLRs.

159
Q

What do NOD-1 and NOD-2 NLRs recognize, and what is their role?

A

NOD-1 and NOD-2 NLRs detect fragments of peptidoglycans from intracellular bacteria. They trigger the production of proinflammatory molecules like tumor necrosis factor (TNF) and interleukin-6 (IL-6).

160
Q

What are inflammasomes, and what do they primarily bind to?

A

Inflammasomes are complexes formed by some NLRs inside cells. They primarily bind to cellular stress-related molecules, a type of damage-associated molecular pattern (DAMP).

161
Q

What is the main role of inflammasomes in the cell?

A

Inflammasomes control the production of inflammatory cytokines, such as interleukin-1β (IL-1β) and IL-18, in response to cellular stress-related molecules.

162
Q

What is the role of cytokines in the immune response?

A

Cytokines are small signaling molecules that play a crucial role in regulating both innate and adaptive immunity by facilitating intercellular communication.

163
Q

How do cytokines affect the inflammatory response, and what are the two categories of cytokines?

A

Cytokines can either promote (proinflammatory) or inhibit (anti-inflammatory) the inflammatory response.

164
Q

Do cytokines mainly act over short or long distances in the body?

A

Cytokines typically act over short distances, but some can have systemic effects, like causing fever.

165
Q

What happens when cytokines bind to target cells?

A

Binding of cytokines to target cells often triggers the synthesis and release of additional cellular products. For example, when tumor necrosis factor-alpha (TNF-α) binds to a cell, it may result in the synthesis and release of interleukin-1.

166
Q

What is a cytokine storm, and what can trigger it?

A

A cytokine storm is an excessive and uncontrolled immune response that generates a large number of proinflammatory cytokines. It can be triggered by infections, malignancies, and other disorders.

167
Q

How does a cytokine storm affect the body, and what can it lead to?

A

A cytokine storm can damage epithelial and endothelial cells, cause vascular leakage, lead to acute respiratory distress syndrome, and affect multiple organ systems.

168
Q

What is the significance of elevated cytokine levels in COVID-19 infection?

A

Elevated cytokine levels in COVID-19 often indicate a poor prognosis and a severe immune response.

169
Q

How does COVID-19 specifically impact the immune response, and what treatment approach involves targeting a specific cytokine?

A

COVID-19 selectively stimulates IL-6 and can lead to lymphocyte exhaustion. One treatment approach is using monoclonal antibodies against IL-6, such as tocilizumab.

170
Q

What are lymphokines and monokines, and what types of cells produce them?

A

Lymphokines are cytokines secreted by lymphocytes, and monokines come from monocytes. However, cytokines are produced by various cell types.

171
Q

What is the role of chemokines, and what type of cells do they primarily attract?

A

Chemokines are a special family of cytokines that primarily attract white blood cells (leukocytes) to sites of inflammation.

172
Q

Which cells produce chemokines, and what triggers their production?

A

Various cells like macrophages, fibroblasts, and endothelial cells produce chemokines. They are produced in response to proinflammatory cytokines like TNF-α.

173
Q

Can you provide examples of chemokines and the types of immune cells they primarily attract?

A

Examples of chemokines include monocyte/macrophage chemotactic proteins (MCP-1, MCP-2, and MCP-3) that attract macrophages, and interleukin-8 (IL-8) that primarily attracts neutrophils.

174
Q

Which cells, when stimulated, primarily produce interleukins (ILs)?

A

Macrophages and lymphocytes are key producers of interleukins in response to stimulation.

175
Q

How many different interleukins (ILs) are there, and what are some of their effects?

A

There are more than 30 different ILs, and they can alter adhesion molecule expression on cells, attract leukocytes to sites of inflammation, promote leukocyte growth in the bone marrow, modulate inflammation, and contribute to the development of the acquired immune response.

176
Q

What is the role of ILs in attracting leukocytes to sites of inflammation?

A

ILs promote chemotaxis, which is the attraction of white blood cells (leukocytes) to the sites of inflammation.

177
Q

How do ILs contribute to the development of the acquired immune response?

A

ILs play a role in the development of the acquired immune response, which is the body’s ability to remember and respond to specific pathogens.

178
Q

What are the two major proinflammatory interleukins, and which cytokine do they cooperate closely with?

A

The two major proinflammatory interleukins are interleukin-1 (IL-1) and interleukin-6 (IL-6), which work closely with another cytokine, TNF-α.

179
Q

Which cells are the main producers of interleukin-1 (IL-1), and how many forms of IL-1 are there?

A

Macrophages primarily produce IL-1, which exists in two forms: IL-1α and IL-1β.

180
Q

What are some effects of IL-1 on various immune cells, including neutrophils?

A

IL-1 activates monocytes, macrophages, and lymphocytes, enhancing both innate and acquired immunity. It also acts as a growth factor for many cell types. Regarding neutrophils, IL-1 induces their proliferation, attracts them to inflammatory sites (chemotaxis), and enhances their ability to kill bacteria.

181
Q

How does IL-1 contribute to the development of fever, and what is it called in this context?

A

IL-1 is an endogenous pyrogen, which means it causes fever. It does so by reacting with receptors on cells in the hypothalamus, affecting the body’s thermostat and resulting in an increase in body temperature.

182
Q

Which cells are the primary producers of interleukin-6 (IL-6)?

A

Macrophages, lymphocytes, and fibroblasts are the main producers of IL-6.

183
Q

What is the role of IL-6 in inflammation and wound healing?

A

IL-6 directly stimulates hepatocytes (liver cells) to produce proteins needed for inflammation (acute-phase reactants) and promotes the growth and differentiation of blood cells in the bone marrow. It also contributes to the growth of fibroblasts, which are essential for wound healing.

184
Q

What cytokine is secreted by macrophages and some other cells in response to TLR stimulation, and what are its main effects?

A

Macrophages and other cells secrete tumor necrosis factor-alpha (TNF-α). TNF-α has various proinflammatory effects, particularly on the vascular endothelium and macrophages.

185
Q

What are the systemic effects of TNF-α when it is secreted in large amounts?

A

In cases of high secretion, TNF-α can induce fever (as an endogenous pyrogen), increase the synthesis of inflammation-related proteins by the liver, and lead to muscle wasting (cachexia) and intravascular thrombosis in severe infections and cancer.

186
Q

What can very high levels of TNF-α, a proinflammatory cytokine, potentially lead to?

A

Very high levels of TNF-α can be lethal and are associated with fatalities from shock caused by Gram-negative bacterial infections.

187
Q

What are anti-inflammatory cytokines, and which two are considered the most important?

A

Anti-inflammatory cytokines reduce the inflammatory response. The most important ones are interleukin-10 (IL-10) and transforming growth factor-beta (TGF-β).

188
Q

Which cells primarily produce interleukin-10 (IL-10), and what does it do to the immune response?

A

Lymphocytes are the main producers of IL-10. IL-10 suppresses the growth of other lymphocytes and the production of proinflammatory cytokines by macrophages. This downregulates both the inflammatory and acquired immune responses.

189
Q

What is the role of transforming growth factors like TGF-β, and what do they induce in response to inflammation?

A

In response to inflammation, various cells produce transforming growth factors like TGF-β. These growth factors stimulate cell division and the differentiation of different cell types, including immature blood cells.

190
Q

What is the role of cytokines in the immune response?

A

Cytokines are small signaling molecules that play a crucial role in regulating both innate and adaptive immunity by facilitating intercellular communication.

191
Q

How do cytokines affect the inflammatory response, and what are the two categories of cytokines?

A

Cytokines can either promote (proinflammatory) or inhibit (anti-inflammatory) the inflammatory response.

192
Q

Do cytokines mainly act over short or long distances in the body?

A

Cytokines typically act over short distances, but some can have systemic effects, like causing fever.

193
Q

What happens when cytokines bind to target cells?

A

Binding of cytokines to target cells often triggers the synthesis and release of additional cellular products. For example, when tumor necrosis factor-alpha (TNF-α) binds to a cell, it may result in the synthesis and release of interleukin-1.

194
Q

What is the role of interferons (IFNs) in the body?

A

Interferons are a family of cytokines that protect against viral infections and help regulate the inflammatory response.

195
Q

How do virally infected cells respond to viral components, and what type of interferons do they produce?

A

Virally infected cells produce type I interferons, primarily IFN-α and IFN-β, in response to viral double-stranded RNA and other viral components (PAMPs).

196
Q

What is the primary function of type I interferons like IFN-α and IFN-β?

A

Type I interferons don’t directly kill viruses. Instead, they induce the production of antiviral proteins and protect neighboring healthy cells.

197
Q

Which type of interferon is mainly produced by lymphocytes, and what does it do in the body?

A

Lymphocytes primarily produce type II interferon, IFN-γ. IFN-γ activates macrophages, enhancing the body’s ability to combat infectious agents, including viruses and bacteria. It also supports the development of acquired immune responses against viruses.

198
Q
A