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Pathology I > Inflammation & Repair > Flashcards

Inflammation & Repair Flashcards

1
Q

how to name inflammatory diseases

A

name of the organ/tissue + “itis” = inflammation in that organ/tissue

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2
Q

classifications of inflammation:

A

-acute or chronic
-exudative or non-exudative
-morphologic patterns (serous, fibrinous, suppurative, ulcerative)

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3
Q

acute inflammation

A

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

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4
Q

chronic inflammation

A

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

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5
Q

ID leukocyte

A

neutrophil
(segmented nucleus)

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6
Q

ID leukocyte

A

plasma cells
(nucleus pushed to the side)

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7
Q

ID leukocyte

A

macrophages
(large, pale-staining)

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8
Q

ID leukocyte

A

lymphocytes
(small, dark staining)

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9
Q

exudative inflammation

A

formation of exudate
-acute inflammation tends to be
more exudative

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10
Q

non-exudative inflammation

A

no formation of exudate
-chronic inflammation is
frequently non-exudative and is often
associated with fibrosis and scarring.

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11
Q

types of injury that can cause inflammation:

A

-thermal
-physical
-chemical
-allergic
-immune mediated disease

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12
Q

inflammation

A

the body’s response to injury

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13
Q

immunity

A

comes into play when inflammation is caused by a LIVING organism (infection)

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14
Q

infection may provoke _____ & ______

A

inflammation and immunity

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15
Q

are inflammation and immunity the same thing?

A

NO

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16
Q

can inflammation exist without infection?

A

yes
-inflammation DOES NOT imply infection

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17
Q

what else can cause inflammation?

A

-hypersensitivity (allergic disease)
-autoimmune diseases

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18
Q

what are the 3 lines of defense for the body?

A
  1. barriers
  2. inflammatory response
  3. immune response
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19
Q

examples of barriers

A

– Skin
– Mucous membranes
– Secretions

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20
Q

examples of inflammatory responses

A

– Cells (leukocytes)
– Molecules (mediators)

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21
Q

examples of immune responses

A

– Antibodies (humoral)
– Cytotoxic T cells (cellular)

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22
Q

where are components of inflammatory responses found?

A
  • Circulating blood cells and plasma proteins
  • Cells of the blood vessel walls
  • Cells and proteins of the extracellular matrix
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23
Q

what are these?

A

components of inflammatory response

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24
Q

where are most of the defensive elements found?

A

blood

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25
Q

inflammation is the means by which what leave the blood and enter the tissue?

A

defensive cells & chemicals

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26
Q

is inflammation beneficial?

A

yes- but excess or prolonged inflammation may be harmful

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27
Q

defensive cells

A

leukocytes

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28
Q

defensive proteins

A

plasma

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29
Q

what are the 5 R’s of the inflammatory response?

A
  • Recognition of the injurious agent
  • Recruitment of leukocytes
  • Removal of the agent
  • Regulation (control) of the response
  • Resolution (repair)
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30
Q

causes of acute inflammation:

A
  • Mechanical injury
  • Chemical injury
  • Radiation injury
  • Thermal injury
  • Infection
  • Compromise of blood supply
  • Immune injury
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31
Q

what are the cardinal signs of inflammation?

A

calor- heat
rubor- redness
tumor- swelling
dolor- pain
functio laesa- loss of function

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32
Q

all that is red (rubor) is not

A

inflammation

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33
Q

what are the cellular events in acute inflammation?

A
  • Margination
  • Rolling
  • Adhesion
  • Diapedesis
  • Chemotaxis
  • Phagocytosis
  • Killing
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34
Q

systemic manifestations of acute inflammation

A
  • Fever – due to pyrogens
    – Cytokines - TNF, IL-1 released by leukocytes
    – Prostaglandins – from membrane phospholipids
  • Leukocytosis
    – Leukemoid reaction
    – Neutrophilia - shift-to-left
    – Lymphocytosis
  • Acute phase response – cytokines stimulate hepatocytes to synthesize and
    secrete acute phase proteins
    – C-reactive protein (CRP) – acts as an opsonin
    – Mannose-binding lectin - acts as an opsonin
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35
Q

lymphangitis

A
  • Lymphatic spread of
    bacterial infection
  • Painful red streaks and
    regional
    lymphadenopathy
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36
Q

chemical mediators of inflammation

A

Preformed mediators:
-histamine
-serotonin

Newly synthesized:
-prostaglandins
-leukotrienes

Factor XII activation:
-kinin system (bradykinin)

Complement activation:
-C3a
-C5a
-C5b-9

37
Q

histamine and serotonin are examples of what?

A

vasoactive amines

38
Q

which mediators are available in preformed supplies?

A

histamine and serotonin

39
Q

where is histamine stored?

A

granules of mast cells

40
Q

where is serotonin stored?

A

granules of platelets

41
Q

what are the first mediators to be released after injury?

A

histamine and serotonin

42
Q

which mediators cause vascular dilation and leakage?

A

histamine and serotonin

43
Q

all acute inflammatory reactions may have one of three outcomes:

A
  1. Complete resolution
  2. Healing by connective tissue replacement
    (fibrosis)
  3. Progression of the response to chronic
    inflammation
44
Q

examples of what type of inflammation?

A

serous inflammation

45
Q

examples of what type of inflammation?

A

fibrinous inflammation

46
Q

examples of what type of inflammation?

A

suppurative (purulent) inflammation

47
Q

examples of what type of inflammation?

A

suppurative (purulent) inflammation

48
Q

abscess

A

A localized collection of pus that has accumulated in
a tissue cavity, producing fluctuance

49
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

50
Q

catarrhal (seromucous) syndrom

A

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

51
Q

ulcerative inflammation

A

an ulcer is a defect in epithelial continuity

52
Q

examples of defects in neutrophil function:

A

-leukocyte adhesion deficiency (LAD)
-lazy leukocyte syndrom
-Chediak-Higashi syndrome
-chronic granulomatous disease of childhood
-myeloperoxidase (MPO) deficiency

53
Q

Chediak-Higashi syndrome

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
54
Q

chronic granulomatous disease of childhood

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 not
    synthesized 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
55
Q

myeloperoxidase (MPO) deficiency

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

56
Q

what is caused by too few neutrophils?

A

-agranulocytosis
-cyclic neutropenia

57
Q

what is caused by failure in adhesion?

A

-leukocyte adhesion deficiency (LAD)

58
Q

what is caused by slow chemotaxis?

A

-lazy leukocyte syndrome

59
Q

what is caused by failure to phagocytose?

A

-Bruton Agammaglobulinemia
-complement deficiency

60
Q

what is caused by failure to kill?

A

-Chediak-Higashi syndrome
-chronic granulomatous disease of childhood
-myeloperoxidase (MPO) deficiency

61
Q

causes of chronic inflammation

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
62
Q

morphologic features of chronic inflammation

A
  • Mononuclear cell infiltration – lymphocytes,
    plasma cells and macrophages
  • Tissue destruction – due to a persistent
    offending agent or by the inflammatory cells
  • Attempts at healing by connective tissue
    replacement - angiogenesis and fibrosis
63
Q
A
64
Q

granulomatous inflammation

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
65
Q

types of giant cells

A

-Langhans giant cells
-foreign body giant cells

66
Q

classification of granulomas

A

-immune granulomas
-foreign body granulomas

67
Q

mycobacterium tuberculosis (intracellular pathogen)

A

blocks fusion of phagosome with lysozome

68
Q

granulation tissue

A

-reparative tissue
-endothelial cells & fibroblasts
-proliferation of blood vessels

69
Q

granulomatous tissue

A

-epitheliod macrophages
-giant cells & lymphocytes

70
Q

example of granulation tissue

A

pyogenic granuloma

71
Q

repair

A
  • Restoration of tissue architecture and function after an injury
  • Repair may occur by regeneration or by healing (scar formation)
72
Q

two mechanisms of tissue repair:

A

-regeneration
-healing

73
Q

regeneration

A

growth of cells and tissues to replace lost structures

74
Q

healing

A

consists of variable proportions of two distinct processes- regeneration and scarring

75
Q

labile cell classification

A

continuously dividing tissues

76
Q

quiescent cell classification

A

stable tissues

77
Q

non-dividing cell classification

A

permanent tissues

78
Q

labile tissues

A
  • Labile cells are derived from the division of stem cells
  • Hematopoietic cells
  • Surface epithelium
  • Stratified squamous epithelium of the skin, mouth,
    pharynx, esophagus, vagina and cervix
  • Gastrointestinal tract epithelium
  • Labile tissues can readily regenerate after injury as long as the
    pool of stem cells is preserved
  • The most common forms of cancer arise from labile tissues:
    – Epidermis – skin cancer
    – Bronchial mucosa – lung cancer
    – Oral mucosa – oral cancer
    – Cervical mucosa – cervical cancer
    – Hematopoietic tissue – leukemias
    Continuously Dividing Tissues – Labile
79
Q

quiescent tissues

A
  • Stable cells are quiescent and have a very low rate of turnover.
  • Replacement is carried out by mitotic division of mature cells.
  • Viscera (liver, kidney, pancreas)
  • Endothelial cells
  • Fibroblasts
  • Smooth muscle cells
    -with the exception of liver, stable tissues have limited capacity to regenerate
    -malignant tumors of stable tissues are among the rarer forms of cancer
80
Q

permanent tissues (non-dividing)

A
  • Permanent cells were generated during fetal
    life and never divide in postnatal life
  • Cannot be replaced if lost
  • Neurons
  • Cardiac myocytes
    -in permanent tissue, repair is dominated by scar formation
81
Q

fibrosis (scarring) occurs if:

A
  • The tissue is intrinsically unable to
    regenerate (heart, brain)
  • The underlying connective tissue scaffolding
    is disrupted
  • Following extensive exudates (organization)
82
Q

objectives of wound healing

A

-epithelial regeneration (restore integrity of the epithelial surface)
-connective tissue repair (restore the tensile strength of the sub-epithelial tissue)

83
Q

healing by primary intention

A

occurs when the wound margins are pulled together

84
Q

what does all wound healing involve?

A

an inflammatory reaction even in the absence of infection

85
Q

healing by secondary intention

A

occurs when the wound margins are NOT pulled together

86
Q

hypertrophic scar

A

excessive scar formation within the boundaries of the original wound producing a raised scar

87
Q

keloid

A

excessive scar formation that grows beyond the boundaries of the original wound

88
Q

what is required for the hydroxylation of proline and lysine?

A

vitamin C

Pathology I (11 decks)

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