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Pathology > Exam III: Inflammation Part II > Flashcards

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

A

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

A

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

A

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

A

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
Q

Acute Inflammation: Complete Resolution

A

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
Q

Acute Inflammation: Connective Tissue Replacement

A

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
Q

Acute Inflammation: Progression

A

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
Q

Vascular Phenomena of Acute Inflammation

A

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
Q

Acute Inflammation: Leukocyte Action

A

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
Q

Chronic Inflammation

A

Inflammation of prolonged duration- weeks or months

May follow acute inflammation or begin insidiously

31
Q

Causes of Chronic Inflammation

A

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
Q

Morphology of Chronic Inflammation

A
  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
  3. 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
Q

Histology of Chronic Inflammation

A

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
Q

Macrophages in Chronic Inflammation

A

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
Q

Tissue Macrophages

A 
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
Q

Monocytes to Macrophages

A

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
Q

Monocyte Migration

A

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
Q

Activated Macrophages

A

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
Q

Lymphocyte: Plasma Cells

A

Lymphocytes
Plasma cells: develop from activated B lymphocytes and produce antibodies
Directed either against persistent foreign or self antigens

40
Q

Eosinophils

A

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
Q

Mast Cells

A

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
Q

Granulomatous Inflammation

A

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
Q

Granuloma

A

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
Q

Granuloma: Epithelioid Cells

A

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
Q

2 Types of Granulomas

A
  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
Q

Acute Phase Response: General Information

A

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
Q

Acute Phase Response: Acute Phase Proteins

A

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
Q

Leukocytosis

A

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
Q

Systemic Effects of Inflammation: Types of Infections

A

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
Q

Systemic Effects of Inflammation: Signs and Symptoms

A 
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
Q

Defective and Excessive Inflammation

A

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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