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Pathophysiology Test 1 > Innate Immunity Inflammation > Flashcards

Innate Immunity Inflammation Flashcards

0
Q 
Innate Immunity (1st line defense)
-Physical Barriers
A

Epithelial Cells of the:

  1. Skin
  2. GI
  3. GU
  4. Respiratory system
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1
Q

Innate Immunity

A
  1. Includes Natural Barriers (physical, mechanical, biochemical)
  2. Inflammation
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2
Q 
Innate Immunity (1st line defense)
-Mechanical
A

Removes bacteria by:

  1. Coughing
  2. Sneezing
  3. Vomiting
  4. Flushing - urine
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3
Q 
Innate Immunity (1st line defense)
-Epithelial Cell-derived Chemicals
A
  1. Lysozyme
    - enzyme attacks the cell walls of GRAM POSITIVE BACTERIA
  2. Cathelicidin / Defensins
    - Antimicrobial peptides that disrupts bacterial membranes and kills them
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4
Q 
Innate Immunity (1st line defense)
-Normal Flora
A
  1. Compete w/ pathogens for nutrition and prevent attachment to epithelium
  2. Helps w/ digestion / produces biotin and Vit K (clotting)
  3. Assits w/ absorption of Ca, Fe, Mg
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5
Q

Innate Immunity: 2nd Line Defense

-Inflammation

A
  1. Protective process
  2. May result from injury, infection
  3. Stimulates healing
  4. Prevent further damage and progressive deterioration
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6
Q

Inflammation

-Signs & symptoms

A
  1. Redness – decreased blood flow & increase RBC concentration to area
  2. Heat – pooling of blood
  3. Swelling – leakage of plasma proteins
  4. Pain - Bradykinin & prostaglandin’s
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7
Q

Inflammation Goals

A
  1. Limit and control the inflammatory process
  2. Prevent and limit infection and further damage
  3. Initiate adaptive immune response
  4. Initiate healing.
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8
Q

Inflammation:

-Development process

A
  1. Damage to Tissue
  2. Vasodilation
  3. Increased Vascular permeability
  4. WBC’s adherence to inner walls of vessels
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9
Q

Cathelicidin

A
  1. Cathelicidin is produced by epithelial cells of the skin, gut, Urinary tract, Respiratory tract
    - Antimicrobial peptides that disrupt bacterial membranes and kills them
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10
Q

Cathelicidins

-Action

A
  1. Bacteria have cholesterol-free cell membranes into which cathelicidin can insert and disrupt the membrane, killing the bacteria
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11
Q

Epithelial Cell-Derived Chemicals

Alpha Defensin’s

A
  1. Often require activation by proteolytic enzymes
  2. Rich in the granules of neutrophils
  3. May contribute to the killing of bacteria by those cells.
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12
Q

Epithelial Cell-Derived Chemicals

Beta Defensins

A
  1. Synthesized in active forms
  2. Can kill bacteria the same way as cathelicidin
  3. Found in epithelial cells lining:
    - respiratory, urinary, and intestinal tracts as well as skin
  4. May help protect epithelial surfaces from infection with adenovirus & HIV
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13
Q

Epithelial Cell-Derived Chemicals

Collectin’s

A
  1. React w/ carbs on the surface of a wide array of pathogenic microorganisms and help cells of the INNATE immune system (MACROPHAGES) recognize and kill microorganisms
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14
Q

Epithelial Cell-Derived Chemicals

-Mannose-Binding lectin (MBL)

A
  1. Powerful activator of a plasma protein system (COMPLEMENT) resulting in damage to bacteria or increased recognition by macrophages
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15
Q

Normal Flora Benefits

A
  1. Digest Fatty acids, large polysaccharides, and other dietary substances
  2. Produce Biotin and Vitamin K
  3. Assist in absorption of ions, such as Ca, Fe, and Vitamin K
  4. Train the adaptive immune system by inducing growth of gut-associated lymphoid tissue (Where cells in the adaptive immune system reside)
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16
Q

Prolonged treatment with Broad-Spectrum Antibiotics

A

Can lead to:

  1. Candida albicans
  2. Clostridium difficile
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17
Q

Opportunistic Microorganisms

A
  1. Can cause disease if the individual’s defenses are compromised
    - Psudomonas aeruginosa
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18
Q

Plasma Protein Systems

A
  1. Complement System
  2. Clotting System
  3. Kinin System
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19
Q

Compliment Cascade

-Overview

A
  1. Factors produced by compliment cascade are among the body’s MOST POTENT defenders against bacterial infection
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20
Q

Compliment Cascade

-Most Important function

A
  1. most important function of the complement cascade is:
    - ACTIVATION OF C3 & C5
  2. Resulting in:
    - Opsonins
    - chemotactic factors
    - anaphylatoxins
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21
Q

Compliment Cascade

-Opsins

A
  1. Coat the surface of bacteria and increase their susceptibility to being phagocytized (eaten) & killed by neutrophils and macrophages
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22
Q

Compliment Cascade

-Chemotactic Factors

A
  1. Diffuse from a site of inflammation and attract PHAGOCYTIC CELLS to that site
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23
Q

Compliment Cascade

-Anaphylatoxins

A
  1. Induce rapid degranulation of mast cells

- release of histamine that induces vasodilation and increased capillary permeability

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24
Q

Compliment Cascade

-Activation of complement components C5b through C9

A
  1. Membrane attack complex

2. Results in a complex that creates pores in outer membrane

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25
Q

Compliment Cascade

-Most potent products

A
  1. C3b (opsonin)
  2. C3a (anaphylatoxin)
  3. C5a (anaphylatoxin, chemotactic factor)
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26
Q

Pathways that control the Activation of Complement (3)

A
  1. Classical Pathway
  2. Lectin Pathway
  3. Alternative Pathway
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27
Q

Pathways that control the Activation of Complement (3)

-Classical Pathway

A
  1. Primarily activated by antibodies (proteins of the acquired immune system)
  2. Antibodies activate the 1st component of complement, C1.
  3. C1 leads to activation of other complement components leading to activation of C3 & C5

Antibodies of the Acquired immune response can use the complement system to kill bacteria and activate inflammation

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28
Q

Pathways that control the Activation of Complement (3)

-Alternative Pathway

A
  1. Activated by several substances found on the surface of infectious organisms (lipopolysaccharides, endotoxin)
  2. Uses Unique proteins (Factor B, D, and properdin) to form complex that activates C3
  3. C3 activation leads to C5 activation and convergence w/ the classical pathway

Can Directly activate complement system by infectious organisms w/out antibody presence ***

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29
Q

Pathways that control the Activation of Complement (3)

-Alternative Pathway (Activation Summary)

A
  1. Directly activate the complement system by presence of certain infectious organisms W/OUT ANTIBODY BEING PRESENT
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30
Q

Pathways that control the Activation of Complement (3)

-Lectin Pathway

A
  1. Similar to classical pathway but is INDEPENDENT OF ANTIBODY
  2. Activated by Mannose-binding lectin (MBL)
  3. MBL is similar to C1 and binds to bacterial polysaccharides containing the carbohydrate mannose
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31
Q

Pathways that control the Activation of Complement (3)

-Summary

A

Complement cascade can be activated by:

  1. Opsonization
  2. Anaphylatoxic activity – resulting in mast cell degranulation
  3. Leukocyte chemotaxis
  4. Cell lysis
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32
Q

Clotting System

-Purpose

A
  1. Plug damaged vessels and stop bleeding
  2. Trap microorganisms and prevent their spread
  3. Provide framework for future repair and healing
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33
Q

Clotting Cascade

-Activation by substances

A

Substances that are released by tissue injury and infection:

  1. Collagen
  2. Proteinases
  3. Kallikrein
  4. Plasmin
  5. Endotoxins (bacterial products)
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34
Q

Clotting Cascade

-Activation Pathways

A
  1. Tissue (Extrinsic) Pathway

2. Contact activation (Intrinsic) Pathway

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35
Q

Clotting System

-Tissue (Extrinsic) Pathway

A
  1. Activated when there is TISSUE INJURY and membrane-bound or soluble tissue factor (TF) (also called tissue thromboplastin), a substance released by damaged ENDOTHELIAL CELLS in blood vessels, REACTS w/ ACTIVATED FACTOR (VIIa)
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36
Q

Clotting System

-Tissue Factor (TF)

A
  1. A substance released by damaged endothelial cells in blood vessels
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37
Q

Clotting System

-Contact Activation (Intrinsic) Pathway

A
  1. Activated w/ abnormal vessel wall and Hageman factor (factor XII) contacts negatively charged SUB-ENDOTHELIAL substances
  2. Killikrein & Kininogen can also activate factor XII
  3. Clotting pathways converge at factor X
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38
Q

Kallikrein & Kininogen

A
  1. Can activate factor XII in the contact activation (intrinsic) pathway
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39
Q

Factor X

A
  1. Activation of factor X begins a common pathway leading to activation of fibrin that polymerizes to form a fibrin clot
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40
Q

Clotting Pathway

-Fibrinopeptides (FP’s)

A
  1. Activation of the clotting cascade produces fragments known as FP’s A & B that enhance the inflammatory response
  2. FP’s are released from fibrinogen when fibrin is produced
    - Both Fibrinopeptides are CHEMOTACTIC for neutrophils and increase vascular permeability by enhancing effects of BRADYKININ.
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41
Q

Kinin Cascade

-Activation

A
  1. Both the clotting and Kinin systems can be initiated through activation of Hageman factor (factor XII) to factor XIIa.
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42
Q

Kinin Pathway

-Prekallikrein

A
  1. Another name for factor XIIa is prekallikrein because it
  2. enzymatically activates the 1st component of the kinin system, prekallikein.
  3. Final products of the kinin cascade is bradykinin
    - produced from a larger precursor molecule, kininogen
43
Q

Kinin Pathway

-Bradykinin

A
  1. Final product of the kinin cascade
  2. Produced from a larger precursor molecule, kininogen
  3. Causes dilation of blood vessels
  4. Acts w/ prostaglandins to induce pain
  5. Causes smooth muscle cell contraction
  6. Increases vascular permeability
44
Q

Plasmin

A
  1. Degrade fibrin polymers in clots
  2. Can also activate the complement cascade through components C1, C3, & C5
  3. Can activate the kinin cascade by activating factor XII and producing prekallikrein activator
45
Q

C1 inh

A
  1. Inhibits complement activation through C1 (Classical pathway )
  2. MASP-2 (lectin pathway), & C3b (alternative pathway)
46
Q

Hereditary Angioedema

A
  1. A genetic defect in C1 inh results in hereditary angioedema, which is a self-limiting edema of cutaneous and mucosal layers resulting from:
    - stress, illness, or relative minor or unapparent trauma
47
Q

PRR’s

A

Pattern Recognition Receptors

  1. Recognize:
    - Pathogen-associated molecular patterns PAMPs
    - Damage-associated molecular patterns DAMPs
48
Q

PAMP

A

Pathogen-associated molecular patterns

1. molecules that are expressed by infectious agents, either found on their surface or released as soluble molecules

49
Q

DAMP

A

Damage-associated molecular patterns

1. Products of cellular damage

50
Q

PRR’s

-Toll-like receptors

A
  1. Primarily recognize a large variety of PAMPs located on the microorganisms cell wall or surface
51
Q

Complement Receptors

A
  1. found on many cells of the innate and acquired immune responses.
  2. Recognize molecules produced by activation of plasma protein systems.
52
Q

Cytokines

A
  1. Variety of secretions that affect other cells to help with cooperation to produce effective protective responses.
  2. Can be either pro-inflammatory or anti-inflammatory.
  3. Usually diffuse over short distances
  4. Some effects of cytokines occur over long distances (FEVER)
53
Q

Interleukins

A
  1. Majority of important cytokines are classified as interleukins or interferons
  2. Produced predominantly by macrophages and lymphocytes in response to stimulation of PRRs or by cytokines
54
Q

Interleukins

-Effects

A
  1. Alteration of adhesion molecule expression on many types of cells
  2. Attraction of leukocytes to a site of inflammation (chemotaxis)
  3. Induction of proliferation and maturation of leukocytes in the bone marrow
  4. General enhancement or suppression of inflammation
55
Q

Interleukin-1 (IL-1)

A
  1. Produced mainly by macrophages
  2. Activates monocytes, other macrophages, and lymphocytes
  3. Enhances both innate and acquired immunity
    - Acts as a growth factor for many cells
  4. Increases # of circulating neutrophils
  5. IL-1 is an endogenous pyrogen
56
Q

IL-1 and Fever

A
  1. IL-1 is an endogenous pyrogen that reacts w/ receptors on cells of the hypothalamus and affects the body’s thermostat resulting in fever
57
Q

IL-6

A
  1. Produced by macrophages, lymphocytes, fibroblasts, and other cells
  2. Directly induces hepatocytes to produce many of the proteins needed in inflammation
  3. Stimulates growth and differentiation of blood cells in the bone marrow and the growth of fibroblasts (required for wound healing)
    3.
58
Q

Tumor necrosis factor-alpha

A
  1. Secreted by macrophages & mast cells in response to stimulation of Toll-like Receptor (TLR)
  2. Pro-inflammatory effects on
    - vascular endothelium and macrophages
59
Q

Tumor Necrosis factor-alpha

-Systemic Effects

A
  1. Inducing fever
  2. Causing increased synthesis of inflammation-related serum proteins by liver
  3. Causing muscle wasting (cachexia)
  4. Very high levels of TNF-alpha can be lethal and are responsible for fatalities from SHOCK caused by gram-negative bacterial infection.
60
Q

INterleukin-10

A
  1. Produced by lymphocytes
  2. Suppresses growth of lymphocytes and the production of pro-inflammatory cytokines by macrophages
  3. Down-regulation of both inflammatory and acquired immune responses
61
Q

Transforming Growth Factors

A
  1. Produced by many types of cells in response to inflammation and induce cell division and differentiation of other cell types, such as immature blood cells
62
Q

Interferons

A
  1. type of cytokine that protect against viral infections
  2. Principal interferons are:
    - INF-alpha
    - INF-Beta
    - INF-Gamma
63
Q

INF

-Action

A
  1. Macrophages and cells that become infected w/ viruses produce and secrete both INF-alpha and INF-beta.
64
Q

INF-alpha & INF-beta

A
  1. Protect the surrounding cells from infection and limit the spread of the virus
65
Q

INF-gamma

A
  1. Produced by lymphocytes;
  2. activates macrophages (increasing microbiocidal activity)
  3. resulting in increased capacity to kill infectious agent
66
Q

Chemokines

A
  1. attract leukocytes to sites of inflammation
    - Leukocyte Chemotaxis
  2. Synthesized by macrophages and endothelial cells in response to pro-inflammatory cytokines
67
Q

Mast Cells

A
  1. MOST IMPORTANT cellular activator of the inflammatory response
  2. Cellular bags of granules located in the loose connective tissues close to blood vessels
    - skin, digestive lining, respiratory tract
68
Q

Basophils

A
  1. Protect mucosal surfaces
  2. Release cell mediators that promote inflammatory response
    - Much like mast cells
69
Q

Leukotrienes

A
  1. Sulfur-containing lipids
  2. Produce histamine-like effects
    - smooth muscle contraction
    - increased vascular permeability
  3. Important in later stages of inflammatory response (prolonged)
70
Q

Prostaglandins

A
  1. Cause increased vascular permeability
    - neutrophil chemotaxis
    - Pain by direct effects on nerves
  2. Long chain, unsaturated fatty acids
71
Q

Prostaglandins E1 & E2

A

Cause increased vascular permeability and smooth muscle contraction

72
Q

Histamine

A
  1. Causes rapid constriction of smooth muscle and dilation of post-capillary venules
  2. Increased vascular permeability
73
Q

Mast Cells

-begin synthesis of..

A
  1. Leukotrienes
  2. Prostaglandins
  3. Platelet activating factor
74
Q

Endothelial Cells

-Action

A
  1. Produce Nitric Oxide (NO) from arginine
  2. Produce prostacyclin from arachidonic acid
  3. Both NO and PGI2 maintain blood flow and pressure and inhibit platelet activation
  4. PGI2 and NO are synergistic
75
Q

Platelets

-Activation

A
  1. Interact w/ components of coagulation cascade to STOP BLEEDING
  2. Degranulation, releasing biochemical mediators like serotonin, which has vascular effects like HISTAMINE
  3. Promote wound healing
76
Q

Platelets

-definition

A

cytoplasmic fragments formed from megakaryocytic

77
Q

Neutrophil

-Primary Role

A
  1. Removal of debris and dead cells in sterile lesions (burns)
  2. Destruction of bacteria in non-sterile lesions
  3. Predominant phagocytes in early inflammatory site
  4. Release macrophage chemotactic factors to attract macrophages to injury site
78
Q

3 Systemic changes associated w/ acute inflammatory response

A
  1. Fever
  2. Leukocytosis (increase in level of circulating leukocytes
  3. Increased level of circulating plasma proteins
79
Q

Pyrogens

A
  1. IL-1 is an endogenous pyrogen released from neutrophils and macrophages
  2. act directly on the hypothalamus
    - area that controls the body’s thermostat
80
Q

Left Shift

A

Leukocytosis-increased number of circulating WBC’s

  1. more immature forms of neutrophils are present in relatively greater than normal proportions
81
Q

Repair Vs. Resolution

A
  1. Repair is when there is replacement of destroyed tissue with scar tissue
  2. Resolution is when there is regeneration of tissues close to normal tissues
82
Q

Cells capable of complete Mitotic Regeneration?

A
  1. Epithelial cells
  2. Hepatic cells
  3. Bone marrow cells
83
Q

Macrophages

A
  1. Engulf Cellular debris, present foreign proteins or antigens to lymphocytes
  2. Arrive 24 hrs or later after neutrophils
84
Q

Monocytes

A
  1. Produced in the bone marrow

2. Enter the circulation and migrate to inflammatory site where they develop into macrophages

85
Q

Neutrophils

A
  1. Move to areas of tissue damage
  2. 1st WBC to arrive at injury/infection site (early inflammation)
  3. Cells are short lived and become component of purulent exudate
86
Q

Eosinophils

A
  1. Important in preventing parasitic infection
  2. Regulation of vascular mediators
    - Limits inflammation
    - Controls vascular effects
  3. Mildly phagocytic
87
Q

Lymphocyte

A
  1. Part of adaptive immune system
  2. Breaks up into T and B lymphocytes
    - T lymphocytes turn into natural killer cells
88
Q

Natural Killer Cells

A
  1. Recognize and eliminate cells infected w/ viruses
  2. Some function in eliminating cancer cells
  3. LINK between innate and adaptive immune system
89
Q

Mast Cells

-Activation

A
  1. Physical & Chemical Injury
  2. Immunologic processes
  3. Toll-like receptors
90
Q

Mast Cells

-Chemicals release in two ways…

A
  1. Degranulation and synthesis of lipid-derived chemical mediators
91
Q

Mast Cell Degranulation

A
  1. Histamine
    - Vasoactive amine causes temporary, rapid constriction of large blood vessels and dilation of post-capillary venules
  2. Retraction of endothelial cells lining capilaries
    - Increases vascular permeability
92
Q

Histamine

-H1 receptor

A
  1. Pro-inflammatory

2. Present in the smooth muscle cells of the bronchi

93
Q

Histamine

-H2 Receptor

A
  1. Anti-inflammatory
  2. Present on parietal cells of the stomach mucosa
    - induces secretion of gastric acid
94
Q

Purulent Exudate

A
  1. Pus: indicates a bacterial infection

- Cysts or abscesses

95
Q

Leukocytosis

A
  1. Increased number of circulating leukocytes

2. Shift to the left

96
Q

Healing

-Reconstructive Phase

A
  1. Fibroblast proliferation
  2. Collagen synthesis
  3. Epithelialization (sealing the wound)
  4. Contraction (shrinking the wound)
  5. Cellular differentiation
97
Q

Healing

-Maturation phase

A
  1. Continuation of cellular differentiation
  2. Scar tissue formation
  3. Scar remodeling
98
Q

Impaired Inflammation in Older adults leads to??

A

Chronic Illness

  1. Diabetes
  2. Cardiovascular
  3. Diabetes
99
Q

Causes of Impaired Inflammation

A
  1. Chronic medication intake
100
Q

Older Adults and Inflammation

A
  1. Impaired inflammation causes chronic disease
  2. Chronic med intake decreases inflammatory response
  3. Healing response is diminished because of skin’s loss of regenerative ability
  4. Infections are more common in older adults
101
Q

Dysfunctional Wound Healing

-Reconstructive phase dysfunction

A
  1. Impaired collagen matrix assembly
    - Keloid scar
    - Hypertrophic scar
  2. Impaired epithelialization
    - Anti-inflammatory steroids, hypoxemia, nutritional deficits
  3. Impaired contraction
    - Contracture
102
Q

Causes of Dehiscence

A
  1. Excessive strain and obesity

- increases risk of wound sepsis

103
Q

Dysfunction during Inflammatory response

-Wound Healing

A
  1. Wound sepsis
  2. Hypovolemia
  3. Hypoproteinemia
  4. Anti-inflammatory steroids
  5. Hemorrhage
  6. Fibrous adhesion
  7. Infection
  8. Excess scar formation
104
Q

Debridement

A
  1. Cleaning up the dissolved clots, microorganisms, erythrocytes, and dead tissue cells
105
Q

Chronic Inflammation

-Characteristics

A
  1. Dense infiltration of lymphocytes and macrophages
  2. Granuloma formation
  3. Epithelioid cell formation
  4. Giant cell formation
  5. Caseous necrosis w/ TB

Pathophysiology Test 1 (10 decks)

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