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Advanced Pathophysiology > Immunity > Flashcards

Immunity Flashcards

(101 cards)

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1
Q

Define innate resistance or immunity.

A

Innate immunity is the first line of defense and includes natural barriers such as the skin and mucous membranes.

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2
Q

What are the key components of the first, second, and third lines of defense?

A

First: Physical and biochemical barriers; Second: Inflammation; Third: Adaptive immunity.

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3
Q

Describe inflammation and how it differs from adaptive immunity.

A

Inflammation is a rapid, non-specific response, while adaptive immunity is specific and slower.

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4
Q

List the microscopic findings of inflammation.

A

Edema, accumulation of white blood cells, and increased permeability.

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5
Q

What are the plasma protein systems involved in inflammation?

A

Complement, coagulation, and kinin systems.

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6
Q

What are the pathways of the complement system?

A

Classical (antibodies), lectin (bacterial carbohydrates), and alternative (pathogen surfaces).

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7
Q

Identify the primary cells involved in inflammation.

A

Mast cells, neutrophils, eosinophils, macrophages.

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8
Q

Explain the role of PRRs, PAMPs, and TLRs in pathogen recognition.

A

PRRs recognize PAMPs, which are common structures in pathogens, TLRs are a type of PRR.

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9
Q

What triggers mast cell degranulation?

A

Injury, immune response, and pathogens can trigger mast cell degranulation.

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10
Q

What are the effects of histamine binding to H1 and H2 receptors?

A

H1: Bronchoconstriction, H2: Secretion of gastric acid.

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11
Q

What are the synthetic products of the mast cell?

A

Leukotrienes, prostaglandins, and platelet-activating factor.

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12
Q

Describe the process of phagocytosis.

A

Steps include recognition, engulfment, formation of phagosome, and destruction.

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13
Q

What roles do neutrophils, macrophages, and eosinophils play in inflammation?

A

Neutrophils remove debris, macrophages initiate repair, eosinophils control inflammation.

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14
Q

What is the role of cytokines in inflammation?

A

Cytokines mediate inflammation, e.g., interleukins and TNF-alpha.

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15
Q

Describe the local signs of acute inflammation.

A

Redness, heat, swelling, pain, and loss of function.

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16
Q

What are the systemic signs of acute inflammation?

A

Fever, leukocytosis, and increased plasma proteins.

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17
Q

What is chronic inflammation and how does it differ from acute inflammation?

A

Chronic inflammation is prolonged and can lead to tissue damage.

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18
Q

What are the phases of wound healing?

A

Hemostasis, inflammation, proliferation, and remodeling.

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19
Q

What are the dysfunctions during wound healing?

A

Ischemia, infection, excess scar formation, wound disruption.

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20
Q

What are the characteristics of pediatric innate immunity?

A

Newborns have depressed inflammatory function and are more susceptible to infection.

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21
Q

Compare natural barriers and biochemical barriers in innate immunity.

A

Natural barriers are physical, while biochemical barriers include secretions like sweat and tears.

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22
Q

What is the role of the skin in the first line of defense?

A

The skin provides a physical barrier and prevents pathogen entry through low pH and tight junctions.

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23
Q

How does the respiratory tract protect against infection?

A

Mucus, cilia, and coughing help clear pathogens from the respiratory tract.

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24
Q

Define adaptive (acquired) immunity.

A

Acquired immunity is slower, specific, and has memory, involving lymphocytes.

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25
Describe the process of complement activation in innate immunity.
Complement activation enhances the ability of antibodies to clear microbes via opsonization and lysis.
26
What is diapedesis and why is it important?
Diapedesis is the movement of leukocytes from blood to tissues through the endothelium.
27
How do neutrophils differ from macrophages?
Neutrophils are first responders, macrophages are long-lasting and initiate repair.
28
Describe the role of TLRs in pathogen recognition.
TLRs recognize PAMPs, leading to an inflammatory response.
29
What is the function of interleukin-1 (IL-1) during inflammation?
IL-1 induces fever and activates the immune response.
30
Explain the significance of opsonization in phagocytosis.
Opsonization tags pathogens for easier recognition and ingestion by phagocytes.
31
How does bradykinin contribute to the inflammatory process?
Bradykinin causes vasodilation, increased permeability, and pain.
32
Identify the differences between acute and chronic inflammation.
Acute inflammation is rapid, while chronic inflammation involves prolonged tissue damage.
33
What role do eosinophils play in parasitic infections?
Eosinophils regulate vascular effects and protect against parasites.
34
Describe the formation of a granuloma during chronic inflammation.
Granulomas form when macrophages fail to eliminate pathogens, forming a fibrotic barrier.
35
What are the main stages of tissue repair during wound healing?
The four stages are hemostasis, inflammation, proliferation, and remodeling.
36
How do fibroblasts contribute to wound healing?
Fibroblasts produce collagen that helps close the wound and restore tissue strength.
37
What are the local manifestations of inflammation?
Redness, heat, swelling, pain, and loss of function are key signs.
38
Explain how leukocyte chemotaxis is regulated.
Chemotaxis is regulated by cytokines and chemical mediators attracting leukocytes.
39
What is the function of the clotting system during inflammation?
The clotting system creates a mesh to limit pathogen spread and promote healing.
40
What are the characteristic symptoms of systemic inflammation?
Fever, elevated WBCs, and increased acute-phase proteins like CRP.
41
How does the body regulate the inflammatory response to prevent excessive tissue damage?
Dendritic cells activate T cells by presenting antigens, linking innate and adaptive immunity.
42
What is the significance of chemotactic factors in inflammation?
Fever is induced by pyrogens acting on the hypothalamus.
43
How do dendritic cells bridge innate and adaptive immunity?
Poor epithelialization can lead to delayed wound healing and infection.
44
Describe how fever is induced during inflammation.
Resolution restores tissue function after inflammation with minimal scarring.
45
What are the consequences of impaired epithelialization during wound healing?
Scar tissue provides strength but lacks the original tissue function.
46
Define the term 'resolution' in the context of wound healing.
Mast cells are found in connective tissues near blood vessels and release histamine.
47
Explain the importance of scar tissue in tissue repair.
Neutrophil chemotactic factor attracts neutrophils to infection sites.
48
What are mast cells and where are they commonly found?
The alternative pathway is triggered by pathogen surfaces like Gram-negative bacteria.
49
What are the effects of neutrophil chemotactic factor?
Collectins bind to microbes, enhancing phagocytosis and clearance by the immune system.
50
What triggers the alternative pathway in complement activation?
Exudates contain cells and proteins that help clear infections and promote healing.
51
What are collectins and what is their role in the immune system?
Histamine increases vascular permeability, causing swelling and redness.
52
Identify and explain the role of exudates in acute inflammation.
A left shift indicates the release of immature neutrophils (bands) in response to infection.
53
How does histamine contribute to vascular changes during inflammation?
Type I interferons (IFN-α, IFN-β) are antiviral, while IFN-γ enhances macrophage activity.
54
Explain the concept of 'left shift' in leukocytosis.
Platelets release growth factors that promote healing and inflammation.
55
What are the two types of interferons and their functions?
Factors like ischemia, infection, or diabetes can impair healing.
56
Describe the role of platelets in inflammation.
Aging reduces the immune response due to lower activity of innate immune cells.
57
What factors can impair the wound healing process?
TLRs recognize microbial patterns and activate the immune response.
58
How does age affect the innate immune response in geriatric populations?
C3a and C5a attract immune cells and promote inflammation.
59
What are Toll-like receptors (TLRs) and their role in innate immunity?
Dendritic cells activate T cells by presenting antigens, linking innate and adaptive immunity.
60
Explain the role of complement fragments C3a and C5a in inflammation.
Fever is induced by pyrogens acting on the hypothalamus.
61
What are the primary functions of lymphocytes in adaptive immunity?
Lymphocytes recognize antigens and activate the adaptive immune response.
62
Explain the impact of diabetes mellitus on wound healing.
Diabetes delays wound healing by impairing blood flow and immune function.
63
What is the function of arylsulfatase in controlling inflammation?
Arylsulfatase helps degrade inflammatory molecules, limiting tissue damage.
64
Describe the events of the vascular response in inflammation.
Vascular events include vasodilation, increased permeability, and leukocyte migration.
65
How does leukocyte adhesion occur during the inflammatory response?
Leukocyte adhesion is facilitated by adhesion molecules like selectins on endothelial cells.
66
What role does nitric oxide play in inflammation?
Nitric oxide relaxes smooth muscle, increasing blood flow and reducing inflammation.
67
Explain the term 'dehiscence' in wound healing.
Dehiscence occurs when a wound ruptures along a surgical incision.
68
What are keloids and how do they form?
Keloids form due to excessive collagen deposition during healing.
69
Identify the role of prostaglandins in the inflammatory process.
Prostaglandins enhance inflammation and also induce pain.
70
What is the role of H2 receptors in the regulation of inflammation?
H2 receptors reduce inflammation by decreasing the release of pro-inflammatory mediators.
71
Describe how ischemia affects the inflammatory response.
Ischemia reduces oxygen supply to tissues, delaying healing and promoting inflammation.
72
What are PAMPs and how do they activate the immune system?
PAMPs are recognized by PRRs, triggering the immune response.
73
How does the complement system interact with other plasma protein systems?
The complement system interacts with coagulation and kinin systems to amplify inflammation.
74
What are the potential complications of wound sepsis?
Wound sepsis can lead to systemic infection, delayed healing, and tissue necrosis.
75
What are the consequences of chronic inflammation?
Chronic inflammation leads to tissue damage, fibrosis, and possible organ dysfunction.
76
Explain how granuloma formation helps in chronic inflammation.
Granulomas wall off foreign material or pathogens that cannot be eliminated.
77
What are the differences between primary and secondary intention wound healing?
Primary intention occurs with minimal tissue loss, secondary involves significant tissue loss.
78
What factors delay wound healing in elderly populations?
Elderly populations have reduced collagen synthesis, poor blood circulation, and immune response.
79
Describe the role of macrophages in tissue repair.
Macrophages clear debris, secrete growth factors, and stimulate fibroblasts for repair.
80
What are the effects of hypovolemia on wound healing?
Hypovolemia reduces blood flow, impairing oxygen and nutrient delivery for tissue repair.
81
What are the primary components of the coagulation system?
The coagulation system forms blood clots and creates a fibrin mesh to limit infection spread.
82
Describe the role of bradykinin in the kinin system.
Bradykinin causes vasodilation, pain, and increased vascular permeability.
83
What are the three main pathways of complement activation?
Classical (antibody-mediated), lectin (mannose-binding), and alternative (pathogen surface).
84
How does the coagulation system help limit the spread of infection?
The coagulation system traps pathogens and prevents their spread to surrounding tissues.
85
What is opsonization and how does it help in the immune response?
Opsonization marks pathogens for phagocytosis by coating them with complement proteins or antibodies.
86
What are the functions of the complement protein C3b?
C3b promotes opsonization and enhances phagocytosis.
87
Describe how leukocyte rolling occurs during inflammation.
Leukocyte rolling is mediated by selectins, which slow down leukocytes along the blood vessel wall.
88
What is the difference between necrosis and apoptosis in tissue injury?
Necrosis is uncontrolled cell death causing inflammation, while apoptosis is programmed cell death.
89
Explain the role of prostaglandins in inflammation and pain.
Prostaglandins promote inflammation and induce pain by sensitizing nerve endings.
90
What are pattern recognition receptors (PRRs) and how do they function?
PRRs detect PAMPs on pathogens and trigger an innate immune response.
91
What are cytokines and chemokines, and how do they differ?
Cytokines mediate immune responses, while chemokines specifically attract immune cells to infection sites.
92
How do neutrophils kill bacteria during an inflammatory response?
Neutrophils engulf bacteria and destroy them using reactive oxygen species and enzymes.
93
What are the roles of T cells in adaptive immunity?
T cells coordinate the adaptive immune response by recognizing and responding to specific antigens.
94
How do natural killer (NK) cells function in innate immunity?
NK cells kill virus-infected or tumor cells by inducing apoptosis.
95
What is the role of macrophages in clearing apoptotic cells?
Macrophages phagocytose apoptotic cells to prevent tissue damage.
96
How does tumor necrosis factor-alpha (TNF-α) contribute to inflammation?
TNF-α promotes inflammation by increasing vascular permeability and recruiting immune cells.
97
What are the systemic effects of interleukin-6 (IL-6)?
IL-6 promotes fever, stimulates acute-phase protein production, and enhances immune cell activation.
98
What are the consequences of excessive complement activation?
Excessive complement activation can lead to tissue damage and autoimmune conditions.
99
Explain the difference between resolution and repair in wound healing.
Resolution restores normal tissue function, while repair involves scar tissue formation.
100
What is the function of fibroblasts in tissue repair?
Fibroblasts produce collagen and extracellular matrix to repair and strengthen damaged tissue.
101

Advanced Pathophysiology (5 decks)

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