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Pathology > Inflammation 1 > Flashcards

Inflammation 1 Flashcards

1
Q

what is inflammation

A

an integrated and tightly controlled set of events associated with the body’s response to:

  • injury
  • infection
  • insult
  • itself
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2
Q

injury

A

trauma

tissue damage/necrosis

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3
Q

infection

A

bacterial
fungal
virus

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4
Q

insult

A 
chemical
radiation
thermal
foreign body
environmental substances
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5
Q

itself

A

autoimmunity to self antigens

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6
Q

cardinal signs of inflammation

A

external manifestations of vascular change and leukocyte recruitment/activation

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7
Q

examples of the cardinal signs of inflammation

A
  • Calor (heat)
  • Rubor (redness)
  • Tumor (swelling)
  • Dolor (pain)
  • Functio laesa (loss of function)
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8
Q

what are the 5 R’s of inflammatory response

A
  • Recognition of injurious agent
  • Recruitment of leukocytes
  • Removal of agent
  • Regulation (control) of response
  • Resolution (repair) of damaged tissue
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9
Q

what happens if injury persists

A

chronic inflammation

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10
Q

what is acute inflammation

A

immediate response (minutes to days)

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11
Q

what is the specificity of acute inflammation

A

limited specificity

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12
Q

characteristics of acute inflammation

A
  • neutrophils

* fluid and plasma exudation

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13
Q

chronic inflammation

A

delayed response (days to years)

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14
Q

specificity of chronic inflammation

A

more specificity

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15
Q

characteristics of chronic inflammation

A
  • lymphocytes & plasma cells

- vascular proliferation and scarring

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16
Q

vascular changes of acute inflammation

A
  • vasodilation

- increased vascular permeability

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17
Q

cellular events of acute inflammation

A
  • neutrophil emigration
  • cellular recruitment
  • activation of neutrophils
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18
Q

what is vasodilation

A

locally increased blood flow due to arteriolar smooth muscle relaxation

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19
Q

vasodilation is mediated by what

A

prostaglandins
histamine
bradykinin

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20
Q

characteristics of vasodilation

A
  • erythema (rumor)

- warmth (calor)

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21
Q

what occurs with increased vascular permeability

A
  • movement of protein-rich fluid into extra-vascular space
  • endothelial contraction (histamine)
  • endothelial disruption (tissue damage)
  • swelling (tumor)
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22
Q

what is effusion

A

-greater than normal volume of fluid within the pericardial, abdominal or pulmonary cavity

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23
Q

classifications of effusion

A
  1. transudate
  2. exudate
    found in pleural or peritoneal cavity
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24
Q

how do differentiate between transudate and exudate

A

-based primarily on the protein [ ]

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25
Q

transudates

A

fluids of non-inflammatory origin with low protein concentration

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26
Q

transudates caused by increased volume caused by alterations in hydrostatic factors as:

A
  • increased venous pressure (heart failure, hepatic cirrhosis with portal hypertension)
  • hypoproteinemia (nephrotic syndrome, protein losing enteropathy)
  • lymphatic blockage
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27
Q

exudates characterized by

A
  • increased protein concentration
  • frequently contain inflammatory cells (turbid0
  • glucose concentration decreased
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28
Q

exudates caused by

A
  • malignancy
  • infection
  • pancreatitis
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29
Q

where can effusion be collected from

A

-chest or abdomen - semi surgical procedures

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30
Q

what is thoracentesis

A
  • collection of effusion through chest wall

- plural fluid

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31
Q

what is paracentesis

A
  • through abdominal wall

- ascitic fluid

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32
Q

what is pericardiocentesis

A
  • collection of effusion from pericardium
  • pericardial fluid
  • not a bedside procedure
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33
Q

what are the mediators of acute inflammatory response

A
  • neutrophils
  • endothelial cells
  • mast cells
  • eosinophils
  • platelets
  • toll like receptors
  • arachidonic acid metabolies
  • complement
  • Hageman factor (Factor XII)
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34
Q

where do mature neutrophils emerge from

A

bone marrow

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35
Q

neutrophils are controlled by

A

chemokines (can circulate in blood for 6-8 h in blood)

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36
Q

what are other clinical names of neutrophils

A
  • polymorphonuclear cells
  • PMNS
  • polys
  • segs
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37
Q

neutrophils are central to acute or chronic inflammation

A

acute

38
Q

action of neutrophils

A

phagocytose microorganisms and tissue debris

39
Q

appearance of neutrophils

A

cytoplasm with granules (primary, secondary, tertiary)

40
Q

what do neutrophils express

A

-selectins and integrins for binding to other cells and to migrate out into interstitum

41
Q

neutrophils express receptors which recognize

A
  • Fc porton of IgG and IgM
  • C5a, C3b and iC3b (complement)
  • cytokines
42
Q

how are neutrophil extracellular traps formed

A

when neutrophils undergo oxidative burst and degranulation

43
Q

what are endothelial cells

A

monolayer of cells lining blood vessels

44
Q

function of endothelial cells

A
  • regulates vascular contraction and relaxation

- regulates platelet aggregation

45
Q

do nonactivated platelets bind normal endothelium

A

no

46
Q

what can endothelial cells express

A

unregulated levels of adhesion molecules (ICAM and VCAM) which can anchor activated neutrophils

47
Q

where are mast cells located

A

adjacent to vessels and widely distributed throughout connective tissue (ie. lug, GI mucosal surfaces, skin)

48
Q

what do mast cells contain

A

preformed histamine granules (aretriolar vasodilation and increased vascular permeability of postcapillary venues)

49
Q

mast cells are activated by

A

-trauma
-cross-linking of cell-surface IgE receptors
C3a and C5a complement proteins

50
Q

what is the immediate response of mast cells

A

release of preformed histamine granules

51
Q

what is the delayed response of mast cells

A
  • arachidonic acid metabolites (leukotrienes)

- second phase of mast cell acute inflammatory response)

52
Q

soon after the release of mast cells it is inactivated by

A

histaminase

53
Q

eosinophils are associated with what type of reaction

A
  • allergic rxn
  • parasite associated rxn
  • acute and chronic inflammatory rxns
54
Q

eosinophils release

A

-cytoplasmic granules with lysosomal enzymes, cytokines and major basic protein (toxic to parasites)

55
Q

platelets are formed from

A

megakaryocytes in bone marrow

56
Q

appearance of platelets

A

bits of cytoplasm (no nucleus)

57
Q

platelets contain

A

inflammatory mediators as dense granules and alpha granules

58
Q

function of platelets

A

promote clot formation

59
Q

toll-like receptors are present on what type of cells

A
  • innate immune system (macrophages, dendritic cells)
  • epithelial cells
  • lymphocytes
60
Q

function of toll-like receptors

A

recognize molecular structures common to microbes

61
Q

TLR activation leads to upregulation of

A

cytokines

62
Q

arachidonic acid is released from

A

phospholipid cell membrane by phopholipases

63
Q

what are arachidonic acid metabolites called

A

eicosanoids

64
Q

arachidonic acid derived from

A

20 carbon F/As

65
Q

what are the 2 main pathways of arachidonic acid

A
  • cyclooxygenase produces prostaglandins

- 5-lipoxygenase produces leukotrienes

66
Q

what factors ofthe cyclooxygenase pathway cause vasodilation and increased vascular permeability

A

PGI2
PGD2
PGE2

67
Q

what mediates pain in the cyclooxygenase pathway

A

PGE2

68
Q

what causes vasoconstriction and platelet aggregation in the cyclooxygenase pathway

A

TXA2

69
Q

what causes neutrophil chemotaxis and activation in the 5-lipoxygenase

A

LTB4

70
Q

what causes smooth muscle contraction (vasoconstriction, brochospasm, increased vascular permeability)

A

LTC4
LTD4
LTE4

71
Q

what causes neutrophil inhibition in 5-lipoxygenase

A

LXA4

LXB4

72
Q

what is complement

A

serum proteins which “complement”/help host defense and inflammation

73
Q

complement proteins C1 to C9 circulate as

A

inactive precursors

74
Q

what is the critical step of complement

A

formation of C3 convertase which cleaves and activates C3

75
Q

C3 cleavage occurs in what 3 pathways

A
  1. alternative pathway
  2. classical pathway
  3. lectin pathway
76
Q

classical pathway

A

C1 complement component binds IgG or IgM bound to antigen

77
Q

alternative pathway

A

microbial cell wall components (ie. endotoxin) directly activates complement

78
Q

lectin pathway

A

plasma lectin binds to mannose residues on microbes (direct pathway)

79
Q

what are the complement disorders

A
  1. hereditary angioedema
  2. paroxysmal nocturnal hemoglobinuria (PNH)
  3. Factor H deficiency
80
Q

what is Hereditary angioedema

A

-deficiency of C1 inhibitor

81
Q

function of C1 inhibitor

A

regulator of various components of clotting, complement and clotting cascade

82
Q

consequences of hereditary angioedema

A
  • increased vascular permeability under skin
  • submucosal and subcutaneous swelling
  • laryngeal edema can lead to death
83
Q

what is paroxysmal nocturnal hemoglobinuria (PNH)

A

-deficiency of decay activating factor (DAF)

84
Q

function of DAF (decay activating factor)

A

normally limits C3 and C5 formation

85
Q

PNH results in

A

complement-mediated lysis of RBCs (Hemolytic anemia)

86
Q

function of factor H

A

normally limits convertase formation

87
Q

Factor H deficiency results in

A
  • higher than normal C3b deposition on endothelium
  • hemolytic uremia syndrome (HUS)
  • spontaneous vascular permeability in macular degeneration of eye
88
Q

what is the product of the kinin system

A

bradykinin

89
Q

what are the direct effects of bradykinin

A
  • increased vascular permeability (very potent)
  • arteriolar dilatation
  • pain
90
Q

bradykinin is inactivated by

A

kininases in plasma and tissue

Pathology (18 decks)

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