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Pathology I > Inflammation > Flashcards

Inflammation Flashcards

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1
Q

Inflammation

A

Caused by same cells that cause cell injury
Potentially damaging
Self-limiting

Elicit a reaction in vascularized CT
Protective response
Eliminates initial cause of injury
Removes necrotic cells/tissue from damage

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2
Q

Self-limiting

A

Resolves itself

Ex: viral infections opposed to bacterial

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3
Q

Three actions of inflammation regarding harmful stimuli

A

Dilutes
Destroys
Neutralizes

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4
Q

Cons of Inflammation

A

Can cause harm
Basis for allergic reactions
Anaphylaxis
Chronic inflammatory disease

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5
Q

What are the key players in inflammation?

A

Leukocytes (WBC)
Plasma proteins
Mast cells
Fibroblasts

All are normally in the blood, but inflammation brings them to injured site

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6
Q

Non-specific defense mechanisms

A

These are non-immune systems

Includes:
Surface membrane barriers
Skin & mucous membranes
Epidermis
Acidity of skin secretions
Mucus secretions trap microorganisms
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7
Q

Surface membrane barrier as

non-specific defense

A

Body’s first line of defense

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8
Q

Skin & mucous membranes as

non-specific defense

A

Epithelium of tissues is intact, then skin and mucous membranes provide physical and chemical protection against most pathogens

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9
Q

Epidermis as

non-specific defense

A

Is a particularly great physical barrier

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10
Q

Acidity of skin secretions as

non-specific defense

A

Inhibits bacterial growth while the sebum in sebaceous glands is toxic to some bacteria

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11
Q

Mucus secretions trap microorganisms as

non-specific defense (example)

A

Stomach mucous secretes hydrochloric acid and pepsin, both of which kill some bacteria

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12
Q

Autoimmunity

A

Inappropriate inflammatory response against the body when no foreign agent present

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13
Q

Non-specific cellular and chemical defenses

A

Pathogens that do not manage to get through the surface membranes may be met by phagocytes

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14
Q

Types of phagocytes in

Non-specific cellular and chemical defenses

A 
Macrophage
Neutrophils
Natural Killer Cells
Plasma Proteins
Interferons
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15
Q

Macrophages

A 
Main type of phagocyte
Work non-specifically in immune system
Have specific names according to their location
Garbage disposal cells
Important for cell maintenance
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16
Q

Neutrophils

A

Work non-specifically in immune system

Become phagocytic upon contact with antigens

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17
Q

Natural Killer Cells

A 
Work non-specifically in immune system
Virus and tumor specialized
Act spontaneously against a greater variety of pathogens
Type of leukocyte
Doe not require activation
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18
Q

Plasma Proteins

A

Work non-specifically in immune system
A group of plasma proteins that are always circulating
When activated, they amplify the inflammatory process
Turned over by the liver

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19
Q

Interferons

A

Work non-specifically in immune system
Proteins released by virus-infected cells
Diffuse to nearby cells
Stimulate them to make proteins
These proteins then inhibit viral replication

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20
Q

Helper T-Cells

A

Critical as it works collaboratively with macrophages
Collections of foreign debris
Ex: HIV

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21
Q

Specific Body Defenses

A

Starts with antigens

Moves to lymphocytes

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22
Q

Antigens

A

Molecules capable of stimulating an immune response.

Each has distinct surface features, or epitopes, resulting in specific responses.

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23
Q

Antibodies

A

Immunoglobins

Y-shaped proteins produced by B cells of the immune system in response to exposure to antigens

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24
Q

Immunity

A

Can be:
innate (natural) or
artificially acquired (adapted)

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25
T Cells
Cytoxic cells Recognizes antigens Kills pathogens
26
T Cells
Cytoxic cells Recognizes antigens Kills pathogens
27
Initial mechanisms of inflammation | & Three major functions
Whether acute or chronic, the initial mechanisms are the SAME. Once a cell body or tissue is injured, the inflammatory reaction will begin. Functions Response will prevent the spread of damaging elements to adjacent tissues Disposes of antigens and dead cells Sets the stage for tissue repair
28
Acute inflammation
Accumulation of fluids and plasma Stimulation of platelets within the vessels Action of leukocytes Occurs over seconds, minutes, hours, days. Begins within seconds of tissue injury Occurs in connective tissue.
29
Sequence of events in acute inflammation
Vascular permeability and edema - Injury causes increased permeability of capillaries in the area - Followed by migration of neutrophils Redness, swelling, heat, pain Vasoconstrictive mediators Cellular response (margination, adhesion, transmigration)
30
5 Cardinal Signs of Inflammation
``` Rubor Tumor Calor Dolor Lack of function ```
31
Neutrophil migration
Cells migrate out of the blood vessels into the CT
32
Increased permeability of capillaries
Endothelial cells contract in response to histamine release | Allows fluid and blood proteins to move into the CT areas that have been injured
33
Vascular permeability and edema
Injury causes increased blood flow to the injured area | Arterioles dilate
34
Rubor
Redness Cardinal sign of inflammation Due to the increased blood flow to the area
35
Tumor
Swelling Cardinal sign of inflammation Due to increased capillary permeability Allows fluid to accumulate in interstitial spaces among cells Rate of fluid entrance to spaces exceeds ability of lymphatic vessels to return the fluid to the venous system Fluid is called exudate
36
Calor
Heat Cardinal sign of inflammation Due to increased blood flow to area
37
Dolor
Pain Cardinal sign of inflammation Due to increased volume of fluid impinges on adjacent sensory nerve endings causing pain
38
Exudate
Fluid involved in swelling Contains clotting factors and antibodies, PLUS inflammatory cells Increased cells Increased plasma proteins Explains swelling Pinches on afferent (sensory) neurons
39
Hydrostatic imbalance
Not inflammatory fluid Other (transudate) fluid Ex: valve problems
40
Vasoconstrictive mediators
In ACUTE inflammation ``` Cells or plasma derivatives: Platelets Mast cells Basophils Leukocytes Injured tissue itself ``` Mediators of increased permeability of the endothelia of blood vessels
41
Platelets
Type of vasoconstrictive mediators Important in clot formation Adhere upon contact with collagen or thrombin
42
Mast Cells
Type of vasoconstrictive mediators Release heparin and histamine Present in connective tissue
43
Basophils
Type of vasoconstrictive mediators In blood circulation Release heparin and histamine
44
Cell response over first 24 hours
Leukocytes move out of blood stream and into CT at the site of injury Chemotactic factors are released from the injury site and cause leukocytes to react in
45
Chemotactic factors
``` Chemical mediators released from the injury site and cause leukocytes to react in: Margination Adhesion Transmigration ```
46
Margination
Leukocytes normally pushed to vessel peripheries against endothelium lining. With endothelial contraction, and increased permeability of capillary walls - leukocytes can slip out of blood vessels and rest against basement membrane of endothelial cells
47
Adhesion
Leukocytes are able to remain stuck to the basement membrane wall instead of returning to blood vessel
48
Transmigration
Leukocytes squeeze through the intercellular space between adjacent endothelial cells
49
Graph of Inflammation - Neutrophils
What you except to see in tissues ``` # of Neutrophils - Slow climb then peaks in hill before chronic phase. Jumps down to very low and levels off. ```
50
Graph of Inflammation - Macrophages
What you except to see in tissues ``` # of Macrophages - Straight slope climb that continues through chronic phase ```
51
Graph of Inflammation - Lymphocytes
What you except to see in tissues ``` # of Lymphocytes - Slow climb, then jump high in chronic phase ```
52
Hemotax
A debris that builds up | Very attracted to neutrophils
53
Chronic inflammation
May follow acute inflammation when acute response can't be resolved (due to persistence of the injurious agent or interference in healing) Lasts weeks, months, or years An active inflammation, tissue injury, and healing going on simultaneously
54
Components of chronic inflammation
Infiltration with mononuclear cells Tissue destruction Repair
55
Infiltration with mononuclear cells | in Chronic inflammation
Such as macrophages and lymphocytes
56
Tissue destruction | in Chronic inflammation
Directed by the inflammatory cells
57
Repair | in Chronic inflammation
Involving new vessel proliferation and fibrosis
58
Settings that chronic inflammation arises
Viral infections Persistent microbial infections (bacteria or fungi) Prolonged exposure to toxic agents Autoimmune diseases
59
Cellular mediators
``` In CHRONIC inflammation Macrophages Lymphocytes Plasma cells Eosinophils Mast cells ```
60
Macrophages | in Chronic inflammation
Mainstay of chronic inflammation mediation Derive from circulating monocytes When monocytes leave bloodstream, travel to injured CT > differentiate into macrophages Capable of phagocytosis When activated, secrete many biologically active products that can result in tissue injury and fibrosis if unchecked
61
Lymphocytes, Plasma cells, Eosinohpils, & Mast cells in Chronic inflammation
Mobilize out of blood stream and into CT | except mast cells which are already in CT
62
What is the classic hallmark of acute inflammation?
Neutrophils
63
Can neutrophils be present in chronic inflammation?
Yes If chronic indicates still extensive neutrophils, then due to either persistent microbes or mediators from macrophages or necrotic cells. Called Acute Chronic Inflammation
64
Granulomatous inflammation
Distinct pattern of chronic inflammation Characterized by: Aggregates of activated macrophages Assume epithelioid appearance
65
Granuloma
Small collection of modified macrophages Have lost motility Stored in encapsulated area along with phagocytize materials Walls off foreign agent
66
Why can granulomas form?
``` In setting of persistent T-cell responses to certain microbes Ex: Tuberculosis Leprosy Syphilis or benign foreign bodies: Sutures Breast implants Splinters ```
67
Foreign body granuloma
A granuloma formed in a foreign body | Ex: suture, implant, splinter, etc.
68
Tissue Repair
Healing is the attempt to resolve damage to tissue | Beings in early inflammatory process
69
Regeneration
Replacement of injured tissue by cells of the same type | This is optimal option
70
Fibrosis
Replacement of injured tissue by connective tissue cells Not optimal, still functional Scarring
71
What type of tissue repair usually occurs?
Both - regeneration and fibrosis
72
Initial repair by CT
Granulation tissue Capillaries bud off from existing ones Protrude at the surface of injury giving granular appearance (picked scab) Can be vascular or fibrous
73
What is the histological hallmark sign of healing from inflammation?
Initial repair by connective tissue
74
What is the appearance of CT repair after inflammation?
Pink Soft Granular appearance due to infiltration of damaged tissue by small blood vessels and fibroblasts
75
What is the end result of granulation?
Scar
76
Vascular vs Fibrous
Vascularity starts to regress and fibroblasts lay down collagen over time. Type I collagen is very densely compacted in fibrosis.
77
Integration of surrounding tissue with scar tissue
Replacement tissue after scarring is at first, or possibly permanent. Both a collagen matrix and surrounding tissue-replacement cells. Ability for replacement by parenchymal cells dependent on magnitude of wound
78
Parenchymal cells
Cells of original injured site Ability to replace depends on magnitude of wound Can replace for integration of surrounding tissue with scar
79
Progression of Scar appearnce
Mat see slight red surface, pink due to vascularity of fibrosis Vasculature then resolves Becomes raised and pink still Then transitions to a white scar
80
Optimal healing
Tissue able to heal | Able to function to full capacity
81
Healing by primary intent
Surgical cuts vs. Jagged cuts Surgical have great advantage - penetrated CT gets platelets activated
82
Tissue Reorganization - Bone
Great ability to heal well Able to scar itself with callous bone Then re-organizes to heal

Pathology I (9 decks)

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