Inflammation and Repair Flashcards

1
Q

Name of the organ or tissue + “itis”

A

= inflammation in that organ or tissue

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

Tonsil =

A

Tonsillitis

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

Appendix =

A

Appendicitis

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

Peritoneum =

A

Peritonitis

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

Lymph Node =

A

Lymphadenitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Salpingitis –

A

fallopian tube

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

Keratitis -

A

cornea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Balanitis –

A

glans penis

– Reiter’s syndrome

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

Cystitis -

A

bladder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

skin -

A

dermatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

nasal mucosa -

A

rhinitis

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

renal glomerulus -

A

glomerulonephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

hair follicle or sebaceous gland -

A

folliculitis

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

paranasal sinus -

A

sinusitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

renal interstitium -

A

pyelonephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

lips -

A

chelitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

ear -

A

otitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

ureter -

A

urethritis, urethritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

oral mucosa

A

stomatitis

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

eyelid -

A

blepharitis

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

urinary bladder -

A

cystitis

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

gingiva -

A

gingivitis

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

conjunctiva -

A

conjunctivitis

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

prostate -

A

prostatitis

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

perdiodontium -

A

periodontitis

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

cornea -

A

keratitis

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

urethra -

A

urethritis

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

dental pulp -

A

pulpitis

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

Classification of Inflammation

3

A
  • Acute or chronic inflammation
  • Exudative or non-exudative inflammation
  • Morphologic Patterns
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Morphologic Patterns

4

A

– Serous
– Fibrinous
– Suppurative
– Ulcerative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Acute inflammation

3

A

– Rapid onset, short duration (minutes to days)
– Emigration of leukocytes, predominately neutrophils
– Exudation of fluid and plasma proteins

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

Chronic inflammation

3

A

– Longer duration
– Mononuclear cells –macrophages, lymphocytes, plasma cells
– Proliferation of blood vessels and fibroblasts

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

Exudative - — inflammation tends to be

more exudative

A

acute

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Non-Exudative - — inflammation is
frequently non-exudative and is often
associated with (2)

A

chronic

fibrosis and scarring

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Inflammation –

A

the body’s response to injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

inflammation (5)

A
– Thermal
– Physical
– Chemical
– Allergic
– Immune mediated disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Immunity –

A

comes into play when inflammation

is caused by a living organism (infection)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Infection may provoke

A

inflammation & immunity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

— may exist without infection

A

Inflammation

–Inflammation DOES NOT imply infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Hypersensitivity (allergic disease) may cause

A

inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Autoimmune disease may cause

A

inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

The Body’s Defenses:

3 Lines of Defense

A

Barriers
Inflammatory Response
Immune Response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Barriers

3

A

– Skin
– Mucous membranes
– Secretions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Inflammatory Response

2

A

– Cells (leukocytes)

– Molecules (mediators)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Immune Response

2

A

– Antibodies (humoral)

– Cytotoxic T cells (cellular)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Components Of
Inflammatory Responses
(3)

A
  • Circulating blood cells and plasma proteins
  • Cells of the blood vessel walls
  • Cells and proteins of the extracellular matrix
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Inflammation Is The

Body’s Response To —

A

Injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Most of the defensive elements are located in the —

A

blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Inflammation is the means by which defensive cells and chemicals leave the blood and enter the —

A

tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Inflammation is a complex reaction to injury:

4

A

– Vascular responses
– Cellular responses
– Systemic reactions
– Repair

51
Q

— is beneficial. Excess or prolonged — may be harmful.

A

Inflammation

52
Q

Leukocytes –

A

defensive cells

53
Q

Plasma –

A

defensive proteins

54
Q

The Inflammatory Response:

5 R’s

A
  • Recognition of the injurious agent
  • Recruitment of leukocytes
  • Removal of the agent
  • Regulation (control) of the response
  • Resolution (repair)
55
Q

Causes of Acute Inflammation

7

A
  • Mechanical injury
  • Chemical injury
  • Radiation injury
  • Thermal injury
  • Infection
  • Compromise of blood supply
  • Immune injury
56
Q

Cardinal Signs of Acute Inflammation

5

A
  • Calor –heat
  • Rubor - redness
  • Tumor - swelling
  • Dolor - pain
  • Loss of function
57
Q

Cellular Events in Acute Inflammation

7

A
  • Margination
  • Rolling
  • Adhesion
  • Diapedesis
  • Chemotaxis
  • Phagocytosis
  • Killing
58
Q

Systemic Manifestations of Acute

Inflammation (3)

A

fever
Leukocytosis
Acute phase response

59
Q

Fever –due to —

A

pyrogens

60
Q

Fever (2)

A

– Cytokines - TNF, IL-1 released by leukocytes

– Prostaglandins –from membrane phospholipids

61
Q

Leukocytosis

3

A

– Leukemoid reaction
– Neutrophilia - shift-to-left
– Lymphocytosis

62
Q

Acute phase response –

A

cytokines stimulate hepatocytes to synthesize and secrete acute phase proteins

63
Q

Acute phase response (2)

A

– C-reactive protein (CRP) –acts as an opsonin

– Mannose-binding lectin - acts as an opsonin

64
Q

Lymphangitis

A

• Lymphatic spread of

bacterial infection

65
Q

Lymphangitis description

A

Painful red streaks and
regional
lymphadenopathy

66
Q

Chemical Mediators Of Inflammation (2) derived

A

cell

plasma protein

67
Q

preformed mediators in secretory granules (3)

A

histamine
serotonin
lysosomal enzymes

68
Q

mediator: histamine
source: (3)

A

mast cells
basophils
platelets

69
Q

mediator: serotonin
source:

A

platelets

70
Q

mediator: lysosomal enzymes
source: (2)

A

neutrophils

macrophages

71
Q

newly synthesized (6)

A
prostaglandins 
leukotrienes 
platelet activating factors
activated oxygen species
NO
cytokines
72
Q

mediator: prostaglandins
source: (3)

A

all leukocytes
platelets
EC

73
Q

mediator: leukotrienes
source:

A

all leukocytes

74
Q

mediator: platelet activating factors
source: (2)

A

all leukocytes

EC

75
Q

mediator: activated oxygen species
source:

A

all lleukocytes

76
Q

mediator: NO
source:

A

macrophages

77
Q

mediator: cytokines
source: (3)

A

lymphocytes
macrophages
EC

78
Q

factor 12 activation (2)

A
kinin system (bradykinin)
coaggulation/fibrinolysis system
79
Q

complement activation (4)

A

C3A
C5A
C3B
C5b-9

80
Q

Vasoactive Amines (2)

A

HISTAMINE AND SEROTONIN

81
Q

Unlike most other mediators, histamine and serotonin are available in

A

preformed supplies

82
Q

Histamine is stored in

A

granules of mast cells

83
Q

Serotonin is stored in the

A

granules of platelets

84
Q

The first mediators to be released after injury

A

Histamine and Serotonin

85
Q

Histamine and Serotonin cause (2)

A

dilation and leakage

86
Q

Antigen (Ag) -

A

A substance that can induce an immune response when introduced into an animal.

87
Q

Antibody (Ab) -

A

A protein that is produced in response an antigen. The antibody binds the antigen that stimulated its production. All antibodies are immunoglobulins.

88
Q

Immunoglobulin (Ig) -

A

A glycoprotein composed of heavy and light chains that functions as an antibody.

89
Q

Schematic Structure of a Typical
Immunoglobulin (Antibody) Molecule
(4)

A
• Heavy chains (2)
• Light chains (2)
• Variable regions form 
antigen-binding site (Fab)
• Constant end (Fc) 
receptor for attachment 
of phagocytic cells)
90
Q

• IgM -

A

first immunoglobulin to appear in an immune response

91
Q

• IgG -

A

principal immunoglobulin of the secondary immune response. Only immunoglobulin capable of crossing the placental barrier

92
Q

• IgA -

A

principal immunoglobulin in external secretions of mucosal surfaces, tears, saliva, and colostrum

93
Q

• IgE -

A

plays an important role in immediate hypersensitivity reactions and parasitic infections

94
Q

• IgD -

A

thought to activate the B-lymphocyte

95
Q

The Complement System

A
• C1 to C9
• Critical step  activation of C3
–C3 convertase cleaves C3 –C3a, C3b
• C3b deposits to microbes surface, forms C5 
convertase
• C5 convertase cleaves C5 –C5a, C5b
• Initiates assembly of MAC
96
Q

Complement System is
Multifunctional
(4)

A
• Membrane attack complex (MAC) lysis 
(C56789)
• Opsonization (C3b)
• Chemotaxis (C5a)
• Vasodilation and increased vessel 
permeability via histamine release  (C3a, C5a) 
anaphylatoxins
97
Q

All acute inflammatory reactions may have one of three outcomes:
(3)

A
  1. Complete resolution
  2. Healing by connective tissue replacement (fibrosis)
  3. Progression of the response to chronic inflammation
98
Q

Fibrinous Inflammation:

A

Fibrinous Pericarditis in Rheumatic Fever

99
Q

Abscess

A

• A localized collection of pus that has accumulated in

a tissue cavity, producing fluctuance

100
Q

Cellulitis

A
• Diffuse spread of an 
acute inflammatory 
process through the 
fascial planes of soft 
tissue producing 
erythema, edema, 
warmth, and pain, 
without consolidation
101
Q

Catarrhal (Seromucous) Inflammation

A
• Catarrhal 
inflammation, a clinical 
type of exudative 
inflammation, occurs 
only on mucosal 
surfaces containing 
mucus-secreting cells, 
such as nasal or 
bronchial mucosa
102
Q

Ulcerative Inflammation:

Recurrent Aphthous Stomatitis

A

• An ulcer is a defect in epithelial continuity

103
Q

Lazy Leukocyte Syndrome

A

Impaired Chemotaxis –Mutation of Contractile Proteins

104
Q

Chediak-Higashi Syndrome

5

A
  • A rare autosomal recessive condition associated with albinism
  • Giant lysosomal inclusions from fused primary granules
  • Both chemotaxis and phagolysosome formation are defective
  • Recurrent infections
  • Platelet function is abnormal
105
Q

Chronic Granulomatous
Disease of Childhood
(5)

A
  • X-linked (2/3) or autosomal (1/3) recessive
  • Deficient NADPH oxidase in the cell membranes of neutrophils and monocytes, resulting in an absent respiratory burst
  • No H2O2 produced - HOCl- is notsynthesized because of the absence of H2O2
  • Catalase-negative organisms (e.g., Streptococcus species) are killed
  • Catalase-positive organisms (e.g., Staphylococcus aureus) are not killed
106
Q

Myeloperoxidase (MPO) Deficiency

5

A
  • A common (1:2,000 individuals) autosomal recessive absence of myeloperoxidase enzyme in neutrophil and monocyte granules
  • Respiratory burst is normal and H2O2 is produced
  • Absence of MPO prevents synthesis of HOCl-
  • No great clinical consequences in most people
  • Diabetics may develop candidiasis
107
Q

Too few neutrophils

2

A

– Agranulocytosis

– Cyclic neutropenia

108
Q

Failure in adhesion

1

A

– Leukocyte Adhesion Deficiency (LAD)

109
Q

Slow chemotaxis

1

A

– “Lazy” leukocyte syndrome

110
Q

Failure to phagocytose

2

A

– Bruton Agammaglobulinemia

– Complement deficiency

111
Q

Failure to kill

3

A

– Chronic Granulomatous Disease of Childhood
– Chediak-Higashi Syndrome
– Myeloperoxidase Deficiency

112
Q

Causes of Chronic Inflammation

8

A
  • Persistent infection - mycobacteria
  • Prolonged exposure to toxic agents
  • Exogenous - silicosis
  • Endogenous - atherosclerosis
  • Immune-mediated inflammatory disease
  • Autoimmune diseases - rheumatoid arthritis
  • Unregulated immune responses against microbes –inflammatory bowel disease
  • Immune responses against environmental substances –(allergic disease) -bronchial asthma
113
Q

Morphologic Features Of
Chronic Inflammation
(3)

A

• Mononuclear cell infiltration
• Tissue destruction
• Attempts at healing by connective tissue
replacement

114
Q

• Mononuclear cell infiltration – (3)

A

lymphocytes,

plasma cells and macrophages

115
Q

• Tissue destruction –

A

due to a persistent

offending agent or by the inflammatory cells

116
Q

• Attempts at healing by connective tissue

replacement - (2)

A

angiogenesis and fibrosis

117
Q

Granulomatous Inflammation

5

A
• A pattern of chronic 
inflammation 
• Aggregates of epitheliod
macrophages (activated)
• Multinucleated giant cells
• Mononuclear leukocytes, 
principally lymphocytes 
and occasionally plasma 
cells peripherally
• Fibrosis variable
118
Q

Classification of Granulomas

2

A
  • Immune granulomas

* Foreign body granulomas

119
Q

Immune Granuloma:

A

Coccidioides immitis

120
Q

Caseation Necrosis in Tuberculosis:

A

Necrotizing Granulomatous

Inflammation

121
Q

Mycobacterium Tuberculosis:

Intracellular Pathogen

A

• Blocks fusion of phagosome with lysozome

122
Q

Granulation Tissue (2)

A

Reparative Tissue

Endothelial Cells and Fibroblasts

123
Q

Granulomatous Tissue (2)

A

Epitheliod Macrophages

Giant Cells

124
Q

Pyogenic Granuloma:

Granulation Tissue NOT — Tissue

A

Granulomatous