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Real Inflammation Flashcards

1
Q

Inflammation

A

Response of living vascularized tissue to injury

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2
Q

Goal of inflammation

A

Remove damaged, necrotic tissues and foreign invaders

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3
Q

Repair

A

Injured tissue is replaced through

  • regeneration of native parenchyma tissue
  • by filling of defect with fibrous tissue
  • both
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4
Q

Cardinal signs of inflammation

A

Rubor -redness
Dolor -pain
Calor - fever
Tumor - swelling

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5
Q

Fifth signs of inflammation

A

Loss of function

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6
Q

2 types of inflammation

A

Acute and chronic

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7
Q

Acute inflammation

A

Rapid onset
Short duration ( hours to days )
Exudation of fluid and plasma proteins leading to edema
Emigration of leukocytes , mostly neutrophils

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8
Q

3 characteristics of acute inflammation

A

> alteration in vascular caliber leading to increased blood flow

> structural changes in micro vascular use to allow plasma cells to get into tissues

> emigration of leukocytes to site of injury , accumulation and activation

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9
Q

Stimuli of acute inflammation

A

Infections

Tissue necrosis ( ischemia , trauma, mechanical injury )

Foreign Bodies

Immune reaction like in hypersensitivity

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10
Q

Changes in vascular flow and caliber

A

Transient constriction for few seconds

Vasodilation ( arterioles and then to the capillaries ) => NO and histamine

Increased permeability

Stasis of blood and more viscous blood

Leukocytes adhesion to endothelium and migrations through the wall

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11
Q

Increased vascular permeability

A

Contraction of endothelial cells

Increased interendothelial cells (histamine, bradykinin, leukotrienes, neuropeptide substance b)

EnDothelial injury

Endothelial cell necrosis and detachment

Transcytosis => increased transport of fluids and proteins

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12
Q

Responses of lymphatic vessels

A

Lymph flow increased to drain edema

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13
Q

How would you have lymphangitis or lymphadenitis in acute inflammation

A

Leukocytes , debris and microbes find their way into the lymph during drainage

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14
Q

Lymphangitis

A

Inflammation of the lymphatic channels because of infection distal to channel

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15
Q

Lymphadenitis

A

Inflammation of the lymph nodes

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16
Q

Recruitment of leukocytes to site of infections

A

Margination
Rolling
Adhesion to endothelium

Migration across endothelium and vessel wall (diapedesis)

Migration into tissue towards chemotactic stimulus

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17
Q

Rolling of leukocytes mediators ( receptors on left, ligand on the right )

A

L-selecting (leukocyte ) —- Glycam-1, CD34 (endothelium)

E-selectin (endothelium ) —- sialyl-lewis X modified protein (leukocytes )

P-selecting (platelet and endothelium ) —- sialyl-lewis X modified protein (leukocytes )

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18
Q

Adhesion of leukocytes mediators (ligand on the right )

A

VLA-4 integrin (leukocyte ) —— VCAM-1 (endothelium)

LFA-1 integrin (leukocyte ) —— ICAM-1 (endothelium)

MAC-1 integrin (leukocyte ) —— ICAM-1 (endothelium)

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19
Q

VLA-4

A

Very late antigen 4

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20
Q

LFA-1

A

Lymphocyte function associated antigen 1

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21
Q

VCAM 1

A

Vascular cell adhesion molecule 1

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22
Q

ICAM 1

A

Intercellular adhesion molecule I

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23
Q

Leukocytes migration through endothelium mediators (ligand on right )

A

PECAM-1 CD31 (endothelium) ——- ligand (leukocyte )

Collagenase (break down basement membrane )

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24
Q

PECAM1 h

A

Platelet endothelial cell adhesion molecule

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25
Q

Chemotaxis

A

Locomotion oriented along a chemical gradient produced by chemoattractants

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26
Q

Exogenous chemoattractants

A

Bacterial products ( peptides with n-formylmethionine) , lipids

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27
Q

Endogenous chemoattractants

A

Cytokines ( IL8)

Complement system C5a

Arachidonic acid metabolites like leukotrienes B4

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28
Q

Chemotaxis process

A

Chemotactic agent binds G protein receptor on leukocyte surface

Signal initiated

Secondary message which increases calcium and activate the Rac/Rho/ cdc42

Polymerizatioj of actin induced which increases its quantity at edge of cell

Leukocyte moved by filopodia towards stimuli

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29
Q

Dominant leukocytes during first 6 to 24 hours of acute inflammation

A

Neutrophils

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30
Q

Leukocyte that replaced neutrophils after 24 hours to 48 hours

A

Monocytes

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31
Q

Who survive longer neutrophils or monocytesu

A

Monocytes

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32
Q

Cellular infiltration that do not have same infiltration pattern in acute inflammation

A

Pseudomonas bacteria - neutrophils dominate for several days

Viral infection - lymphocytes may

Some hypersensitivity rxns- eosinophils dominant

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33
Q

Recognition of microbes and dead tissues by

A

Toll like receptors

G protein coupled receptors on macrophages, neutrophils and other leukocytes

Receptors for opsinins

Receptors for cytokines

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34
Q

Toll like receptors recognize

A

Bacteria lipopolysaccharide (LPS)

Bacterial Proteoglycans and lipids

Unmethylated CpG nucleotides

dsDNA viral

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35
Q

G protein coupled receptors on macrophages, neutrophils and other leukocytes recognize…

A

Small bacterial peptide with n formylmethionyl

Chemokines

Product of complement such as c5a

Lipid mediators

PGs

Leukotrienes

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36
Q

Receptors for opsinins recognize

A

Antibodies

Complement proteins

Lectins

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37
Q

Opsonization

A

Coating of particle to make it more disgestable through phagocytosis

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38
Q

Receptors for cytokines recognize

A

Cytokines (inf-y)

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39
Q

Removal of offending agents in acute inflammation

A 
Phagocytosis : 
Recognition and attachment 
Particle engulfment 
Vacuole formation with particle inside 
Killing and degradation of particle
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40
Q

In acute inflammation, how is engulfed particle killed

A

ROS (superoxide ion)

Reactive nitrogen species ( NO, peroxynitrite)

Enzymes like elastase

Microbicidal granules (defensins, lactoferrin, lysozyme, Cathelicidins)

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41
Q

What leukocytes when activated promote proliferation of endothelial cells and fibroblasts , and synthesis of collagen

A

Macrophages

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42
Q

Leukocytes induced injury

A

Collateral damage as part of normal defense reaction

In appropriate target of Inflammatory response

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43
Q

Leukocyte induced injury examples

A

Acute respiratory distress syndrome with neutrophils

Acute transplant rejection by lymphocytes antibodies and complement

Asthma by eosinophils IGE antibodies

Glomerulonephritis By neutrophils monocytes antibodies complement

Septic shock by cytokines

Like abscess by neutrophils and bacteria

Arthritis by lymphocytes macrophages and antibodies

Atherosclerosis by macrophages and lymphocytes

Chronic transplants rejection by lymphocytes and cytokines

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44
Q

Leukocytes genetic defects

A

Leukocyte adhesion deficiency 1
Leukocyte adhesion deficiency 2
Chronic granulomatous disease=> decreased oxidative burst
X linked => phagocyte oxidase membrane component
Autosomal recessive => phagocyte oxidase cytoplasmic component
MPO deficiency => decreased microbial killing because deficient MPO
Chediak higashi syndrome

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45
Q

Leukocyte adhesion deficiency 1

A

Mutation in beta chain CD11/CD18 integrans - defective leucocyte adhésion

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45
Q

Genetic defect in leukocytes function

A 
Leukocytes adhesion deficiency 1 leukocyte adhesion deficiency 2 Chronic granulomatosis disease
 X linked 
Autosomal recessive
MPO Deficiency
Chediak higashi syndrome
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46
Q

Leukocyte adhesion deficiency 2

A

Mutation in fucosyl transferase fr synthesis of sialylated oligosaccharadise - defective leucocyte adhésion

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47
Q

Chronic granulomatosis disease X linked

A

Decreased oxidative burst due to Phagocytes oxidase (membrane components)

48
Q

Chronic granulomatosis disease Autosomal recessive

A

Decreased oxidative burst due to phagocyte oxidase but cytoplasmic component

49
Q

MPO deficiency

A

Defect in macrophages causing decreased microbial clearance

50
Q

Chediak higashi syndrome

A

Decreased leukocyte function due to mutations

Affect protein involved involved in lysosomal membrane traffic

51
Q

Acquired defects in leukocyte function

A

Bone marrow suppression ( tumors , radiation, chemotherapy) - production of leukocyte

Diabetes, malignancy, sepsis , chronic dialysis - adhesion, chemotaxis

Leukemia, anemia, sepsis, diabetes, malnutrition - phagocytosis , microbicidal activity

52
Q

Mediators of inflammation for termination

A

Produced in rapid bursts when stimuli present

Short half lives

Degraded after release

54
Q

Cytokines released by macrophages for anti inflammation response

A

IL 10

TGF BETA

55
Q

Anti inflammatory lipid mediators

A

Resolvins

Protectins

56
Q

Neural impulses in antiinflammation

A

Cholinergic discharge

Inhibit production of TNF in macrophages

57
Q

Types of mediators of inflammation

A

Cell derived mediators

Plasma protein derived mediators

58
Q

Cell derived mediators of acute inflammation

A 
Platelets 
Neutrophils 
Monocyte macrophages 
Mast cells
Mesenchymal cells ( endothelium, smooth muscle , fibroblasts ) 
Ahh
59
Q

Plasma protein derived mediators

A

Complement proteins
Kinins
Present in blood as inactive precursors

60
Q

Cell derived mediators that release HISTAMINE

A

Mast cells
Basophils
Platelets

61
Q

Histamine action

A

Vasodilation
Increased permeability
Endothelial activation

62
Q

Cell derived mediators that release serotonin

63
Q

Role of serotonin

A

Vasodilation

Increased permeability

64
Q

Cell derived mediators that release prostaglandins

A

Mast cell , leukocyte

65
Q

Prostaglandins role

A

Vasodilation
Pain
Fever

66
Q

Cell derived mediators that release leukotriene

A

Mast cell

Leukocytes

67
Q

Leukotriene action

A

Increased vascular permeability
Chemotaxis
Leukocyte adhesion And Activation

68
Q

Cell derived mediators that release platelet activating factors

A

Leukocytes

Mast cells

69
Q

Platelet activating factor role

A 
Vasodilation 
Increased vascular permeability 
Leukocyte adhesion 
Chemotaxis 
Degranulation 
Oxidative burst
70
Q

Cell derived mediators that release ROS

71
Q

ROS role

A

Killing of microbes

Tissue damage

72
Q

Cell derived mediators that release nitric oxide

A

Endothelium

Macrophages

73
Q

Nitric oxide role

A

Vascular smooth muscle relaxation

Killing of microbes

74
Q

Cell derived mediators that release chemokines

A

Leukocytes

Activated macrophages

75
Q

Chemokines roles

A

Chemotaxis

Leukocytes activation

76
Q

Cell derived mediators that release cytokines ( TNF, IL1)

A

Macrophages
Endothelial cells
Mast cells

77
Q

Cytokines roles ( TNF , IL1)

A

Local endothelial activation with expression of adhesion molecule

Fever
Pain
Anorexia
Hypotension
Decrease vascular resistance
78
Q

Fibroblast effects of acute inflammation

A 
Increased : 
Proliferation of fibroblasts
Collagen synthesis 
Collagenase
Protease 
PGE synthesis
79
Q

Cell derived mediators that release neuropeptides ( substance P and neurokinin A)

A

Sensory nerves

Various leukocytes

80
Q

Role of neuropeptides

A

Initiation and propagation of inflammatory response
Increase vascular permeability
Pain

81
Q

Plasma protein derived mediators that release complement products (C5a, C3a, C4a)

A

Plasma produced in liver

82
Q

Complement products role

A

Leucocyte chemotaxis and activation

Vasodilation by mast cell stimulation

83
Q

Plasma protein derived mediators that release kinins

A

Plasma produced by liver

84
Q

Kinin role

A

Increased vascular permeability
Smooth muscle contraction
Vasodilation
Pain

85
Q

Proteases activated during coagulation

86
Q

Proteases action

A

Endothelial activation

Leukocyte recruitment

87
Q

Classical complement pathway

A

C1 —> activated C1
Activated C1 —> C4bC2b
C4bC2b —C3 convertase —> C4bC2bC3b

C4bC2bC3b —C5 convertase—> C5-9 MAC complex

88
Q

Lectin pathway

A

C1 —mannose binding lectin —> activated C1
Activated C1 —> C4bC2b
C4bC2b —C3 convertase —> C4bC2bC3b

C4bC2bC3b —C5 convertase—> C5-9 MAC complex

89
Q

Alternative pathway

A

C3 —> C3b

C3b — factor B and D —> C3bBb —> C3bBb3b —> C5 convertase—> C5-9 MAC complex

90
Q

Fate of complement activation

A

Destruction of microbe by leukocytes (C5a, C3a)

Phagocytosis of microbe (C3b)

Mac complex lysis of microbe

91
Q

Outcomes of chronic inflammation

A

Complete resolution

Healing by connective tissue (fibrosis )

Progression to chronic inflammation

92
Q

Morphology pattern of acute inflammation

A

Dilation small blood vessels

Slowing of blood flow

Accumulation of leukocytes in extra vascular tissue

Accumulation of fluid in extra vascular tissue

93
Q

Special morphological features of acute inflammation

A 
Serous inflammation 
Fibrinous inflammation 
Suppurative or purulent inflammation 
Abscess 
Ulcers
94
Q

Serous inflammation

A

Outpouring of thin fluid ( effusion) that may be derived from plasma or from secretions of mesothelioma cells lining serous cavities ( peritoneal , pleural , pericardial )

95
Q

Example of serous inflammation

A

Skin blister

96
Q

Fibrinous inflammation

A

Due to very increase in vascular permeability
Large molecule like fibrinogen pass vascular barrier
Fibrin deposited in extra cellular space
Occurs in large vascular leaks or in presence of procoagulant stimulus

Found in body cavities that

97
Q

Fibrinous inflammation histology

A

Fibrin -> eosinophilic mesh work of threads or amorphous coagulum

98
Q

Fibrinous exudate removal

A

Fibrin removed by Fibrinolysis

Other debris by macrophages s

99
Q

What happens if fibrin not removed

A

Stimulate ingrowth of fibroblast

Leads to scarring

100
Q

Organization of fibrin

A

Conversion of fibrin to scar tissue

101
Q

Suppurative or purulent inflammation

A

Production of large amount of pus or purulent exudate

Plus contains neutrophils, nécrose cells , edema fluid

102
Q

Pyogenic bacteria

A

Bacteria that cause suppurative inflammation with formation of pus

103
Q

Abscesses

A

Localized collection of purulent inflammatory tissue due to suppuration buried in tissue
Due to deep seeding of bacteria into tissue

104
Q

Abscess histology

A

Central region with mass of necrotic leukocytes and tissue cells

Some of preserved neutrophils around necrosis

Around it , vascular dilation parenchymal and fibroblastic proliferation occur

105
Q

Fate of abscess

A

Walled off

Replaced by connective tissue

106
Q

Ulcers

A

Local defect, excavation of surface of an organ or tissue

Produced by shedding of inflammatory necrotic tissue

Exist when tissue necrosis and resultant inflammation occur on tissues surface or near it

107
Q

Most common site of ulcers

A

Mucosa of the mouth, stomach, intestines , genitourinary tract

Skin and subcutaneous tissue of lower extremeties in older persons

108
Q

Chronic inflammation

A

May follow acute inflammation or insidious from onset

Longer duration (weeks or months) with active inflammation, tissue destruction, attempts at repair

109
Q

Main factors of chronic inflammation

A

Lymphocytes and macrophages

Proliferation of blood vessels

Fibrosis

Tissue destruction

110
Q

Conditions with insidious onset of chronic inflammation

A

Rheumatoid arthritis
Atherosclerosis
Tuberculosis
Pulmonary fibrosis

111
Q

Causes of chronic inflammation

A

Persistent infections of difficult microorganism to eradicate

Immune mediated inflammatory disease ( autoimmune disease , unregulated immune response against microbes , response against common substances)

Prolonged exposure to potentially toxic agents
Endogenous ( toxic lipid) , exogenous ( silica)

112
Q

Morphology of chronic inflammation

A

Infiltration:
mononuclear ( macrophages , lymphocytes )
plasma cells ( eosinophilia and mast cells )

Tissue destruction ( persistent offending agent or inflammatory cells )

Attempts at healing by connective tissue ( fibrosis )

Proliferation of small blood vessels by angiogenesis

113
Q

Role of macrophages in chronic inflammation

A 
Help in inflammation and tissue injury : 
ROS and NOS 
Proteases 
Cytokines , chemokines 
Coagulation factors 
AA metabolites 
Repair : 
Growth factors 
Fibrogenic cytokines 
Angiogenic factors 
Remodeling collagenesis
114
Q

Granulomatois inflammation

A

Distinctive pattern of chronic i
Inflammation

Formation of granulomas in inflammation ( cellular attempt to contain offending agent difficult to eradicate)
Strong activation of T lymphocytes -> macrophages activation

115
Q

Main disease with granulmatois inflammation

A

Tuberculosis

Sarcoidosis 
Leprosy
Syphilis
Mycotic infections 
Irritant lipids
Autoimmune disorders
116
Q

Systemic effect of inflammation

A 
Acute phase response : 
Fever 
High acute phase proteins ( C reactive protein, fibrinogen, serum) 
Leukocytosis ( neutrophilia, lymphocytes is, eosinophilia) 
Leukopenia ( typhoid fever, viruses, rickettsia, protozoa, TB) 
High pulse 
High blood pressure
Decreased sweating 
Rigors 
Chills 
Anorexia 
Somnolence
Malaise 
Disseminated intravascular coagulation 
CDV failure 
Metabolic disturbance 
Septic shock
117
Q

Consequence of defective inflammation

A

Increased infection

delayed wound healing

118
Q

Consequence of excessive inflammation

A 
Allergies 
Autoimmunity 
Atherosclerosis 
IHD 
Neurodégénérative disease like alzheimer

mechanism of disease (22 decks)

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