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PATHOLOGY EXAM 1 > inflammation and repair 3 > Flashcards

inflammation and repair 3 Flashcards

1
Q

what are the morphologic patterns for the classification of inflammation

A

serous
fibrinous (clots)
suppurative (pus)
ulcerative

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2
Q

describe acute inflammation

A

-rapid onset, short duration (mins to days)
-emigration of leukocytes[mainly neutrophils]
-exudation of fluid and plasma proteins

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3
Q

describe chronic inflammation

A

-longer duration
-mononuclear cells (macrophages, lymphocytes, plasma cells)
-proliferation of blood vessels and fibroblasts

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4
Q

acute inflammation tends to be more (exudative/non-exudative)

A

exudative [fluid present]

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5
Q

chronic inflammation is frequently (exudative/non-exudative) and is often associated with: _______and______

A

non-exudative

fibrosis and scarring

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6
Q

what are the bodies 5 responses to injury:

A

known as inflammation
1. thermal
2. physical
3. chemical
4. allergic
5. immune mediated disease

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7
Q

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

A

immunity

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8
Q

T/F
inflammation and immunity are not the same thing

A

TRUE

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9
Q

____may provoke inflammation and immunity

A

infection

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10
Q

what exists without infection

A

inflammation

(inflammation does NOT imply infection)

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11
Q

these may cause inflammation :
1. (allergic disease)
2.

A
  1. hypersensitivity
  2. autoimmune disease
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12
Q

the body’s 3 lines of defense

A
  1. barriers (physical)
  2. inflammatory response
  3. immune response
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13
Q

what are the physical barriers of the body

A

skin
mucous membranes
secretions

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14
Q

what are the body’s inflammatory response (non-specific)

A

cells (leukocytes)
molecules (mediators)

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15
Q

what are the body’s immune response (specific)

A

antibodies (humoral)
cytotoxic t cells (cellular)

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16
Q

where are the components of the inflammatory responses found in:
1
2
3

A
  1. circulating blood cells and plasma proteins
  2. cells of the blood vessel walls
  3. cells and proteins of the ECM
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17
Q

where are most of the defensive elements located in the body

A

in the blood

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18
Q

process where defensive cells and chemicals leave the blood and enter the tissue

A

inflammation

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19
Q

inflammation is a complex reaction to injury and 4 responses include:

A
  1. vascular responses
  2. cellular responses
  3. systemic reactions (fever)
  4. repair
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20
Q

defensive cells:

A

leukocytes
WBC

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21
Q

defensive proteins

A

plasma

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22
Q

the inflammatory response 5 R’s:

A
  1. recognition of the injurious agent
  2. recruitment of leukocytes
  3. removal of the agent
  4. regulation (control) of the response
  5. resolution (repair)
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23
Q

cardinal signs of inflammation
1
2
3
4
5

A
  1. calor-heat
  2. rubor-redness
  3. tumor-swelling
  4. dolor-pain
  5. loss of function
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24
Q

list the cellular events in acute inflammation:

A
  1. margination (cells line up on peripheral)
  2. rolling
  3. adhesion
  4. diapedesis (squeeze between cells to get into connective tissue)
  5. chemotaxis
  6. phagocytosis
  7. killing
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25
Q

3 systemic manifestations of acute inflammation

A

fever- due to pyrogens
leukocytosis
acute phase response- cytokines stimulate hepatocytes to synthesize and secrete acute phase proteins

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26
Q

Fever [due to pyogenes], which is a systemic manifestation of acute inflammation, utilizes

A

cytokines [TNF, IL-1 released by leukocytes]
and
prostaglandins [from membrane phospholipids]

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27
Q

leukocytosis which is a systemic manifestation of acute inflammation, utilizes

A

-leukemoid reaction
-neutrophilia (shift to left)
-lymphocytosis

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28
Q

acute phase response[cytokines stimulate hepatocytes to synthesize and secrete phase proteins] which is a systemic manifestation of acute inflammation, utilizes

A
  • c-reaction protein (CRP) :acts as an opsonin
  • mannose-binding lectin: acts as an opsonin
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29
Q

lymphatics in inflammation:

A

lymphangitis

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30
Q

lymphatic spread of bacterial infection. painful red streaks and regional lymphadenopathy

A

lymphatics in inflammation: lymphangitis

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31
Q

what are the first mediators after inflammation, which are vasoactive amines

A

histamine and serotonin

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32
Q

this mediator is stored in granules of mast cells

A

histamine

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33
Q

this mediator is stored in the granules of platelets

A

serotonin

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34
Q

what do the mediators histamine and serotonin cause

A

cause vascular dilation and leakage

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35
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
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36
Q

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

A

abcess

37
Q

diffuse spread of an acute inflammatory process through the fascial planes of soft tissue producing erythema, edema, warmth, and pain, without consolidation

A

cellulitis

38
Q

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

A

caterrhal (seromucous) inflammation

39
Q

an ulcer is a defect in epithelial continuity

A

ulcerative inflammation: recurrent aphthous stomatitis (like canker sores)

40
Q

leukocyte adhesion deficiency-LAD is an example of

A

defects in neutrophil function
(basically severe periodontitis)

41
Q

impaired chemotaxis- mutation of contractile proteins, is known as:
which is a defect in neutrophil function

A

lazy leukocyte syndrome

42
Q

rare autosomal recessive condition associated with albinism

A

chediak-higashi syndrome

43
Q

chediak-higashi syndrome defects:

A
  1. giant lysosomal inclusions from fused primary granules
  2. both chemotaxis and phagolysosome formation are defective
  3. recurrent infections
  4. platelet function is abnormal
44
Q

deficient NADPH oxidase in the cell membranes of neutrophils and monocytes, resulting in an absent respiratory burst

A

chronic granulomatous
-disease of childhood

45
Q

in chronic granulomatous (disease of childhood) what is not produced, which results in HOCL- not being synthesized because of the absence of this

A

no H2O2 produced

46
Q

in chronic granulomatous (disease of childhood), what are the catalase-negative organism and what are the catalase-positive organisms

A

catalase-negative organisms: streptococcus species are killed

catalase-positive organisms: staphylococcus species are NOT killed

47
Q

common autosomal recessive absence of myeloperoxidase enzyme in neutrophil and monocyte granules

A

myeloperoxidase (MPO) deficiency

48
Q

autosomal disease where respiratory burst is normal and H2O2 is produced

A

(MPO) myeloperoxidase deficiency

49
Q

the absence of MPO in (MPO) myeloperoxidase deficiency disease, prevents the synthesis of ______.
no great clinical consequences in most and diabetics may develop candidiasis

A

HOCL-

50
Q

list the 5 immune deficiencies caused by defects in leukocyte function

A
  1. too few neutrophils
  2. failure in adhesion
  3. slow chemotaxis
  4. failure to phagocytose
  5. failure to kill
51
Q

examples of too few neutrophils which is caused by defects in leukocyte function

A

agranulocytosis and cyclic neutropenia

52
Q

example of failure in adhesion which is caused by defects in leukocyte function

A

leukocyte adhesion deficiency (LAD)

53
Q

example of slow chemotaxis which is caused by defects in leukocyte function

A

lazy leukocyte syndrome

54
Q

examples of failure to phagocytose which is caused by defects in leukocyte function

A
  1. bruton agammaglobulinemia
  2. complement deficiency
55
Q

examples of failure to kill which is caused by defects in leukocyte function

A
  1. chronic granulomatous disease of childhood
  2. chediak-higashi syndrome
  3. myeloperoxidase deficiency
56
Q

morphologic features of chronic inflammation

A
  1. mononuclear cell infiltration (lymphocytes, plasma cells and macrophages)
  2. tissue destruction (due to a persistent offending agent or by the inflammatory cells)
  3. attempts at healing by connective tissue replacement (angiogenesis and fibrosis)
57
Q

a pattern of chronic inflammation. aggregates of epitheliod macrophages (activated).
multinucleated giant cells
-mononulcear leukocytes, principally lymphocytes, and occasionally plasma cells peripherally
-fibrosis variable

A

granulomatous inflammation

58
Q

2 classifications of granulomas

A

immune granulomas and foreign body granulomas

59
Q

fungal infection inside giant cells; type of immune granuloma

A

coccidioides immitis

60
Q

blocks fusion of phagosome with lysozome

intracellular pathogen

A

mycobacerium tuberculosis

61
Q

granulation tissue vs granulomatous tissue

-reparative tissue
-endothelial cells and fibroblasts
-perliferation of blood vessels

A

granulation tissue

62
Q

granulation tissue vs granulomatous tissue

-epitheliod macrophages
-giant cells

A

granulomatous tissue

63
Q

pyogenic granuloma is a type of (granulation tissue/ granulomatous tissue)

A

granulation tissue

64
Q

restoration of tissue architecture and function after an injury

A

repair

65
Q

repair may occur by _____ or by _____(scar formation)

A

regeneration or healing

66
Q

growth of cells and tissues to replace lost structures

A

regeneration

67
Q

consists of variable proportions of two distinct processes:

A

healing
regeneration and scarring

68
Q

regeneration cell classification:
1
2
3

A
  1. continuously dividing tissues- labile
  2. stable tissues- quiescent
  3. permanent tissues- non-dividing
69
Q

continuously dividing tissues -labile cells- are derived from the division of

A

stem cells

70
Q

types of continuously dividing tissues (labile)

A

-hematopoietic cells
-surface epithelium
-stratified squamous epithelium of the skin, mouth, pharynx, esophagus, vagina and cervix
-gastrointestinal tract epithelium

71
Q

____tissues can readily regenerate after injury as long as the pool of stem cells is preserved

A

labile tissues (continuously dividing tissues)

72
Q

____ cells are quiescent and have a very low rate of turnover

A

stable cells

73
Q

replacement of stable cells is carried out by

A

mitotic division of mature cells

74
Q

types of stable tissues

A

-viscera (liver, kidney, pancreas)
-endothelial cells
-fibroblasts
-smooth muscle cells

75
Q

___cells were generated during fetal life and never divide in postnatal life

A

permanent tissues (non-dividing)

76
Q

these cells cannot be replaced if lost
-neurons; cardiac myocytes

A

permanent tissues (non-dividing)

77
Q

in permanent tissues, repair is dominated by

A

scar formation

78
Q

fibrosis (scarring) occurs if:

A
  1. the tissue is intrinsically unable to regenerate (heart, brain)
  2. the underlying connective tissue scaffolding is disrupted
  3. following extensive exudates (organization)
79
Q

two objectives of wound healing

A

epithelial regeneration
connective tissue repair

80
Q

restore integrity of the epithelial surface

A

epithelial regeneration (wound healing)

81
Q

restore the tensile strength of the sub-epithelial tissue

A

connective tissue repair (wound healing)

82
Q

this healing occurs when the wound margins are pulled together

A

healing by primary intention

83
Q

with healing by primary intention, all wound healing involves an ________even in the absence of infection

A

inflammatory reaction

84
Q

healing by secondary intention, healing by secondary union occurs when

A

the wound margins are NOT pulled together

85
Q

granulation tissue cells

A

endothelial cells
fibroblasts
myofibroblasts- contractile

86
Q

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

A

hypertrophic scar

87
Q

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

A

keloid
-common in african americans

88
Q

this is required for the hydroxlyation of proline and lysine

A

vitamin C

PATHOLOGY EXAM 1 (12 decks)

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