Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pathology I > Inflammation > Flashcards

Inflammation Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Self-limiting

A

Resolves itself

Ex: viral infections opposed to bacterial

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Three actions of inflammation regarding harmful stimuli

A

Dilutes
Destroys
Neutralizes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Cons of Inflammation

A

Can cause harm
Basis for allergic reactions
Anaphylaxis
Chronic inflammatory disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Surface membrane barrier as

non-specific defense

A

Body’s first line of defense

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Epidermis as

non-specific defense

A

Is a particularly great physical barrier

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Autoimmunity

A

Inappropriate inflammatory response against the body when no foreign agent present

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Types of phagocytes in

Non-specific cellular and chemical defenses

A 
Macrophage
Neutrophils
Natural Killer Cells
Plasma Proteins
Interferons
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Neutrophils

A

Work non-specifically in immune system

Become phagocytic upon contact with antigens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Helper T-Cells

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Specific Body Defenses

A

Starts with antigens

Moves to lymphocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Antigens

A

Molecules capable of stimulating an immune response.

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Antibodies

A

Immunoglobins

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Immunity

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

T Cells

A

Cytoxic cells
Recognizes antigens
Kills pathogens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

T Cells

A

Cytoxic cells
Recognizes antigens
Kills pathogens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Initial mechanisms of inflammation

& Three major functions

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Acute inflammation

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Sequence of events in acute inflammation

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

5 Cardinal Signs of Inflammation

A 
Rubor
Tumor
Calor
Dolor
Lack of function
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Neutrophil migration

A

Cells migrate out of the blood vessels into the CT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Increased permeability of capillaries

A

Endothelial cells contract in response to histamine release

Allows fluid and blood proteins to move into the CT areas that have been injured

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Vascular permeability and edema

A

Injury causes increased blood flow to the injured area

Arterioles dilate

34
Q

Rubor

A

Redness
Cardinal sign of inflammation
Due to the increased blood flow to the area

35
Q

Tumor

A

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
Q

Calor

A

Heat
Cardinal sign of inflammation
Due to increased blood flow to area

37
Q

Dolor

A

Pain
Cardinal sign of inflammation
Due to increased volume of fluid impinges on adjacent sensory nerve endings causing pain

38
Q

Exudate

A

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
Q

Hydrostatic imbalance

A

Not inflammatory fluid
Other (transudate) fluid
Ex: valve problems

40
Q

Vasoconstrictive mediators

A

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
Q

Platelets

A

Type of vasoconstrictive mediators
Important in clot formation
Adhere upon contact with collagen or thrombin

42
Q

Mast Cells

A

Type of vasoconstrictive mediators
Release heparin and histamine
Present in connective tissue

43
Q

Basophils

A

Type of vasoconstrictive mediators
In blood circulation
Release heparin and histamine

44
Q

Cell response over first 24 hours

A

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
Q

Chemotactic factors

A 
Chemical mediators
released from the injury site and cause leukocytes to react in:
Margination
Adhesion
Transmigration
46
Q

Margination

A

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
Q

Adhesion

A

Leukocytes are able to remain stuck to the basement membrane wall instead of returning to blood vessel

48
Q

Transmigration

A

Leukocytes squeeze through the intercellular space between adjacent endothelial cells

49
Q

Graph of Inflammation - Neutrophils

A

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
Q

Graph of Inflammation - Macrophages

A

What you except to see in tissues

# of Macrophages - 
Straight slope climb that continues through chronic phase
51
Q

Graph of Inflammation - Lymphocytes

A

What you except to see in tissues

# of Lymphocytes - 
Slow climb, then jump high in chronic phase
52
Q

Hemotax

A

A debris that builds up

Very attracted to neutrophils

53
Q

Chronic inflammation

A

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
Q

Components of chronic inflammation

A

Infiltration with mononuclear cells

Tissue destruction

Repair

55
Q

Infiltration with mononuclear cells

in Chronic inflammation

A

Such as macrophages and lymphocytes

56
Q

Tissue destruction

in Chronic inflammation

A

Directed by the inflammatory cells

57
Q

Repair

in Chronic inflammation

A

Involving new vessel proliferation and fibrosis

58
Q

Settings that chronic inflammation arises

A

Viral infections
Persistent microbial infections (bacteria or fungi)
Prolonged exposure to toxic agents
Autoimmune diseases

59
Q

Cellular mediators

A 
In CHRONIC inflammation
Macrophages
Lymphocytes
Plasma cells
Eosinophils
Mast cells
60
Q

Macrophages

in Chronic inflammation

A

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
Q

Lymphocytes, Plasma cells, Eosinohpils, & Mast cells in Chronic inflammation

A

Mobilize out of blood stream and into CT

except mast cells which are already in CT

62
Q

What is the classic hallmark of acute inflammation?

A

Neutrophils

63
Q

Can neutrophils be present in chronic inflammation?

A

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
Q

Granulomatous inflammation

A

Distinct pattern of chronic inflammation
Characterized by:
Aggregates of activated macrophages
Assume epithelioid appearance

65
Q

Granuloma

A

Small collection of modified macrophages
Have lost motility
Stored in encapsulated area along with phagocytize materials
Walls off foreign agent

66
Q

Why can granulomas form?

A 
In setting of persistent T-cell responses to certain microbes
Ex: 
Tuberculosis
Leprosy
Syphilis
or benign foreign bodies:
Sutures
Breast implants
Splinters
67
Q

Foreign body granuloma

A

A granuloma formed in a foreign body

Ex: suture, implant, splinter, etc.

68
Q

Tissue Repair

A

Healing is the attempt to resolve damage to tissue

Beings in early inflammatory process

69
Q

Regeneration

A

Replacement of injured tissue by cells of the same type

This is optimal option

70
Q

Fibrosis

A

Replacement of injured tissue by connective tissue cells
Not optimal, still functional
Scarring

71
Q

What type of tissue repair usually occurs?

A

Both - regeneration and fibrosis

72
Q

Initial repair by CT

A

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
Q

What is the histological hallmark sign of healing from inflammation?

A

Initial repair by connective tissue

74
Q

What is the appearance of CT repair after inflammation?

A

Pink
Soft
Granular appearance due to infiltration of damaged tissue by small blood vessels and fibroblasts

75
Q

What is the end result of granulation?

A

Scar

76
Q

Vascular vs Fibrous

A

Vascularity starts to regress and fibroblasts lay down collagen over time.

Type I collagen is very densely compacted in fibrosis.

77
Q

Integration of surrounding tissue with scar tissue

A

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
Q

Parenchymal cells

A

Cells of original injured site

Ability to replace depends on magnitude of wound

Can replace for integration of surrounding tissue with scar

79
Q

Progression of Scar appearnce

A

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
Q

Optimal healing

A

Tissue able to heal

Able to function to full capacity

81
Q

Healing by primary intent

A

Surgical cuts vs. Jagged cuts

Surgical have great advantage - penetrated CT gets platelets activated

82
Q

Tissue Reorganization - Bone

A

Great ability to heal well
Able to scar itself with callous bone
Then re-organizes to heal

Pathology I (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions