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Exam III: Inflammation Part II Flashcards

1
Q

Plasma Protein Derived Mediators

A

Three interrelated systems: complement, kinin, and clotting systems

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2
Q

Complement System: General Information

A

Consists of more than 20 proteins numbered C1 through C9
Functions in both innate and adaptive immunity for defense against microbial pathogens
Several cleavage products of complement proteins are elaborated
Causes increased vascular permeability, chemotaxis, and opsonization
Critical step in complement activation= proteolysis of the third (and most abundant) component, C3

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3
Q

Complement System: Inflammation

A

Inflammation
C3a, C5a, and, to a lesser extent, C4a are cleavage products of the corresponding complement
Stimulate histamine release from mast cells to increase vascular permeability and cause vasodilation
C3a, C5a, and C4a are called anaphylatoxins

C5a: powerful chemotactic agent for neutrophils, monocytes, eosinophils, and basophils
Activates the lipoxygenase pathway of AA metabolism in neutrophils and monocytes
Causes further release of inflammatory mediators

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4
Q

Complement System: Phagocytosis

A

Phagocytosis
C3b and its cleavage product iC3b (inactive C3b)
When fixed to a microbial cell wall, act as opsonins
Promote phagocytosis by neutrophils and macrophages

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5
Q

Complement System: Cell Lysis

A

Cell lysis

Deposition of the MAC on cells causing the cells permeable to water and ions resulting in death (lysis) of the cells

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6
Q

C3a and C5a

A

Most important inflammatory mediators
Can be cleaved by several proteolytic enzymes present within the inflammatory exudate including plasmin and lysosomal enzymes released from neutrophils, which initiate a self-perpetuating cycle of neutrophil recruitment
Directly self perpetuate the inflammatory process

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7
Q

Complement Activation and Effector Functions

A

Alternative Pathway (microbe triggered), Classical Pathway (Ab triggered), and Lectin Pathway (mannose binding lectin triggered) converge at the step where C3b is deposited on the microbe causing the following effector functions:

  1. C3a and C5a causes inflammation
  2. C3b/C3bi causes phagocytosis
  3. Formation of MAC causes lysis of microbes
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8
Q

Coagulation and Kinin Systems

A

Culminate in the activation of thrombin and the formation of fibrin

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9
Q

Intrinsic Clotting Pathway

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Series of plasma proteins activated by Hageman factor (factor XII), which is a protein synthesized by the liver that circulates in an inactive form and activated upon contact with negatively charged surfaces

initiated by chemicals released from platelets and collagen, which activates 12a, 11a, 9a, 10a, 2a/thrombin, 1a/fibrin, and stabilized fibrin (activated in that order)

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10
Q

Kinin

A

Vasoactive peptides derived from plasma proteins (kininogens)

Action of specific proteases (kallikreins)
Active form of factor XII (factor XIIa)
Converts plasma prekallikrein into an active proteolytic form (kallikrein) and cleaves a plasma glycoprotein precursor high-molecular-weight kininogen, to produce bradykinin

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11
Q

Bradykinin

A 
Increases vascular permeability
Causes contraction of smooth muscle
Dilation of blood vessels
Pain when injected into the skin
Short-lived---quickly inactivated by an enzyme called kininase
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12
Q

Fibrinolytic System

A

At the same time factor XIIa is inducing fibrin clot formation, it activates the fibrinolytic system
Cascade counterbalances clotting by cleaving fibrin
Solubilizing the clot

Kallikrein: cleaves plasminogen, which is a plasma protein that binds to the evolving fibrin clot to generate plasmin and a multifunctional protease

Fibrinolytic system: primary function of plasmin that lyses fibrin clots
Cleaves the complement protein C3 to produce C3 fragments
Degrades fibrin to form fibrin split products
Activate Hageman factor to trigger multiple cascades

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13
Q

Summary of Mediators

A

Bradykinin, C3a, and C5a: mediators of increased vascular permeability
C5a: mediator of chemotaxis
Thrombin: effects on endothelial cells and many other cell types

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14
Q

C3a and C5a

A

C3a and C5a: generated by several types of reactions
Immunologic reactions, involving antibodies and complement (the classical pathway)
Activation of the alternative and lectin complement pathways by microbes, in the absence of antibodies
Agents not directly related to immune responses
Plasmin, kallikrein, and some serine proteases

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15
Q

Activated Hageman Factor

A

Activated Hageman factor (factor XIIa): initiates four systems (inflammatory response)

  1. Kinin system: produces vasoactive kinins
  2. Clotting system: induces formation of thrombin
  3. Fibrinolytic system: produces plasmin and degrades fibrin to produce fibrinopeptides
  4. Complement system: produces anaphylatoxins and other mediators
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16
Q

Morphologic Hallmarks of Acute Inflammation

A

Morphologic hallmarks of acute inflammation:

Dilation of small blood vessels= increased permeability
Slowing of blood flow
Accumulation of leukocytes and fluid in extravascular tissue

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17
Q

Serous Inflammation

A

Marked by outpouring of thin fluid

Derived from plasma/secretions of mesothelial cells
Peritoneal, pleural, and pericardial cavities
Accumulation of fluid in these cavities= effusion

Skin blister: burn or viral infection causing a large accumulation of serous fluid

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18
Q

Examples of Serous Inflammation

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Serous effusion of the right pleural cavity – clear, straw colored fluid meaning you can see through it and it is yellowish

Chylous effusion of the peritoneal cavity meaning that it is lymphatic fluid- either a rupture of lymphatic vessel

Blood in the pleural cavity – hemothorax NOT a pleural effusion

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19
Q

Fibrous Inflammation

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Fibrinous exudate
Vascular leaks are large
Local procoagulant stimulus (e.g., cancer cells)
Characteristic of inflammation: lining of body cavities like the meninges, pericardium and pleura

Microscopic examination: fibrin appears as an eosinophilic (very pink) meshwork of threads (dropped butter example)
Amorphous coagulum
Removed by fibrinolysis and clearing of other debris by macrophages

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20
Q

Consequences of Fibrin not Removed

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If fibrin is not removed: stimulates ingrowth of fibroblasts and blood vessels and leads to scarring
Conversion of the fibrinous exudate to scar tissue (organization)
Pericardial sac: opaque fibrous thickening of the pericardium and epicardium and obliteration of the pericardial space and affect heart beat

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21
Q

Suppurative Inflammation

A

Large amounts of purulent exudate containing neutrophils, liquefactive necrosis, and edema fluid
Bacteria (e.g., staphylococci) produce this localized suppuration- pyogenic (pus-producing) bacteria
Example: acute appendicitis
Also occurs in meninges, bowl, abdominal cavity, etc.
Can look very yellow or green

22
Q

Suppurative Inflammation: Abscesses

A

Abscesses: localized collections of purulent inflammatory tissue; usually centrally located
Suppuration buried in a tissue, an organ, or a confined space produced by deep seeding of pyogenic bacteria into a tissue
Debris in tissue can easily fall out during autopsy

Appears as mass of necrotic leukocytes and tissue cells
Necrotic focus…microscopic examination
Around it—zone of preserved neutrophils
Outside it—vascular dilation and parenchymal and fibroblastic proliferation

23
Q

Ulcers

A

Local defect, or excavation, of the surface of an organ or tissue
Produced by the sloughing (shedding) of inflamed necrotic tissue
Most commonly encountered in mucosa of the mouth, stomach, intestines, or genitourinary tract; also, skin and subcutaneous tissue of the lower extremities, especially in older persons who have circulatory disturbances
Laryngeal ulceration from intubation
Diabetes patients with atherosclerosis - cutaneous ulcers
Gangrenous necrosis with a large cutaneous ulceration

24
Q

Acute Inflammation: Variables

A

Variables that may modify the basic process of inflammation
1. Nature and intensity of the injury
2. Site and tissue affected
3 Responsiveness of the host- immune system status

25
Acute Inflammation: Complete Resolution
Restoration of site of acute inflammation to normal, which is a usual outcome Injury is limited or short-lived and there is little tissue destruction The damaged parenchymal cells can regenerate Removal of cellular debris and microbes by macrophages Resorption of edema fluid by lymphatics
26
Acute Inflammation: Connective Tissue Replacement
Healing by connective tissue replacement Fibrosis: occurs after substantial tissue destruction, and the inflammatory injury involves tissues that are incapable of regeneration Abundant fibrin exudation in tissue or serous cavities that cannot be adequately cleared Connective tissue grows into the area of damage Converts it into a mass of fibrous tissue Organization
27
Acute Inflammation: Progression
Progression of the response to chronic inflammation May follow acute inflammation Response may be chronic from the onset Injurious agent cannot be defeated Acute to chronic transition Acute inflammatory response cannot be resolved due to persistence of injurious agent or interference with normal process of healing Example: bacterial infection of the lung Focus of acute inflammation (pneumonia) Extensive tissue destruction and formation of a cavity Chronic lung abscess
28
Vascular Phenomena of Acute Inflammation
Characterized by increased blood flow to the injured area Results mainly from arteriolar dilation and opening of capillary beds Induced by mediators such as histamine Increased vascular permeability Accumulation of protein-rich extravascular fluid (exudate) Plasma proteins leave the vessels (widened interendothelial cell junctions of the venules) Redness (rubor), warmth (calor), and swelling (tumor) Increased blood flow and edema
29
Acute Inflammation: Leukocyte Action
Circulating leukocytes adhere to the endothelium via adhesion molecules Traverse the endothelium and migrate to the site of injury under the influence of chemotactic agents Activated leukocytes release toxic metabolites and proteases extracellularly Causes tissue damage Prostaglandins, neuropeptides, and cytokines released Local symptom---pain (dolor)
30
Chronic Inflammation
Inflammation of prolonged duration- weeks or months | May follow acute inflammation or begin insidiously
31
Causes of Chronic Inflammation
Persistent infections by microorganisms such as mycobacteria, and certain viruses, fungi, and parasites Immune reaction (delayed-type hypersensitivity) Immune-mediated inflammatory diseases Autoimmune diseases- never starts as acute inflammation Atherosclerosis: chronic inflammatory process of the arterial wall induced by endogenous toxic plasma lipid components
32
Morphology of Chronic Inflammation
1. Infiltration with mononuclear cells: macrophages, lymphocytes, and plasma cells 2. Tissue destruction: induced by the persistent offending agent or by the inflammatory cells 3 Proliferation of small blood vessels: angiogenesis 4. Fibrosis Mononuclear cells- NOT neutrophils Not seeing a ton of extra blood flow and not really much proliferation of small blood vessels, only due to fibrosis process and tissue repair, not enough to create red swollen area
33
Histology of Chronic Inflammation
Chronic inflammation as demonstrated by infiltrating lymphocytes and plasma cells: Plasma cells have eccentrically placed nucleus "clock faced" Lymphocyte: little cytoplasm with centrally located nucleus
34
Macrophages in Chronic Inflammation
Component of the mononuclear phagocyte system, also known as the reticuloendothelial system Consists of closely related cells of bone marrow origin Blood monocytes differentiate to tissue macrophages
35
Tissue Macrophages
``` Tissue macrophages are diffusely scattered in the connective tissue Liver (Kupffer cells) Spleen Lymph nodes (sinus histiocytes) Lungs (alveolar macrophages) Central nervous system (microglia) ```
36
Monocytes to Macrophages
Mononuclear phagocytes Arise from a common precursor in the bone marrow Gives rise to blood monocytes From the blood, monocytes migrate into tissues Half-life of blood monocytes is about 1 day Differentiate into macrophages Life span of tissue macrophages is several months or years
37
Monocyte Migration
Monocytes emigrate into extravascular tissues early in acute inflammation Within 48 hours--predominant cell type When it reaches the extravascular tissue… Undergoes transformation into the macrophage Activated by a variety of stimuli: microbial products, cytokines, other chemical mediators
38
Activated Macrophages
Products of activated macrophages Serve to eliminate injurious agents (microbes) Initiate the process of repair Responsible for tissue injury in chronic inflammation Activation of macrophages Increased levels of lysosomal enzymes and reactive oxygen and nitrogen species Production of cytokines, growth factors, and other mediators of inflammation Tissue destruction: hallmark of chronic inflammation *Overall, macrophages can contribute to inflammation and injury as well as repair
39
Lymphocyte: Plasma Cells
Lymphocytes Plasma cells: develop from activated B lymphocytes and produce antibodies Directed either against persistent foreign or self antigens
40
Eosinophils
Abundant in immune reactions and mediated by IgE Parasitic infections Chemokine for eosinophil recruitment: eotaxin Granules that contain major basic protein Highly cationic protein that is toxic to parasites Causes lysis of mammalian epithelial cells Benefit in controlling parasitic infections Contribute to tissue damage in immune reactions and allergies Eosinophils are usually red in appearance when under a microscope with many granules
41
Mast Cells
Widely distributed in connective tissues Participate in acute and chronic inflammatory reactions Degranulation and release of mediators: Histamine and prostaglandins Allergic reactions to foods, insect venom, or drugs Catastrophic results (e.g. anaphylactic shock)
42
Granulomatous Inflammation
Distinctive pattern of chronic inflammation Cellular attempt to contain an offending agent that is difficult to eradicate Strong activation of T lymphocytes leading to macrophage activation Cause injury to normal tissues Tuberculosis (most common), Sarcoidosis, Cat-scratch disease, Lymphogranuloma inguinale, Leprosy, Brucellosis, Syphilis, Mycotic infections, Berylliosis
43
Granuloma
Focus of chronic inflammation Consists of a microscopic aggregation of macrophages Transformed into epithelium-like cells Surrounded by a collar of mononuclear leukocytes like lymphocytes and occasionally plasma cells Body is trying to eradicate using epithelial like cells See a zone of leukocytes/lymphocytes… sometimes see plasma cells but mostly lymphocytes
44
Granuloma: Epithelioid Cells
Epithelioid cells- "epithelial like" Pale pink granular cytoplasm Indistinct cell boundaries Fuse to form giant cells in the periphery or center of granulomas and may attain diameters of 40 to 50 μm
45
2 Types of Granulomas
1. Foreign body granulomas: incited by relatively inert foreign bodies, and forms around material Talc (IV drug abuse), sutures- foreign material can be identified in the center of the granuloma (refractile) 2. Immune granulomas: caused by a variety of agents that are capable of inducing a cell-mediated immune response Produces granulomas usually when the inciting agent is poorly degradable or particulate Prototype is caused by infection with Mycobacterium tuberculosis- granuloma is referred to as a tubercle Presence of central caseous necrosis rare in other granulomatous diseases
46
Acute Phase Response: General Information
Collectively called the acute-phase response, also known as the systemic inflammatory response syndrome Reactions to cytokines whose production is stimulated by bacterial products Consists of several clinical and pathologic changes Fever: elevation of body temperature (1° to 4°C), and one of the most prominent manifestations produced in response to substances called pyrogens
47
Acute Phase Response: Acute Phase Proteins
Consists of several clinical and pathologic changes Acute-phase proteins: plasma proteins synthesized in the liver Concentrate in the plasma in response to inflammatory stimuli Three best-known proteins to check for in blood work: C-reactive protein (CRP) Fibrinogen Serum amyloid A (SAA) protein
48
Leukocytosis
Consists of several clinical and pathologic changes Leukocytosis: common feature of inflammatory reactions, especially those induced by bacterial infections Leukocyte count usually climbs to 15,000 or 20,000 cells/μL, but may reach extraordinarily high levels of 40,000 to 100,000 cells/μL Leukemoid reactions: similar to the white cell counts observed in leukemia Accelerated release of cells from the bone marrow causes a rise in the number of more immature neutrophils in the blood (shift to the left)
49
Systemic Effects of Inflammation: Types of Infections
Bacterial infections: increase in the blood neutrophil count (neutrophilia) Viral infections (infectious mono, mumps, and German measles): absolute increase in the number of lymphocytes (lymphocytosis) Bronchial asthma, allergy, and parasitic infestations: increase in the absolute number of eosinophils (eosinophilia) Infections (typhoid fever and viruses, rickettsiae, and certain protozoa): decreased number of circulating white cells (leukopenia)
50
Systemic Effects of Inflammation: Signs and Symptoms
``` Increased pulse and blood pressure Decreased sweating Redirection of blood flow from cutaneous to deep vascular beds Minimizes heat loss through the skin Rigors (shivering) Chills (search for warmth) Anorexia Somnolence ```
51
Defective and Excessive Inflammation
Defective inflammation Results in increased susceptibility to infections Associated with delayed wound healing Provides the necessary stimulus to get the repair process started Excessive inflammation Basis of many types of human disease Allergies Disorders in which the fundamental cause of tissue injury is inflammation

Pathology (14 decks)

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