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General Pathology > Acute inflammation > Flashcards

Acute inflammation Flashcards

1
Q

what is inflammation?

A

Inflammation is the response of the body’s vascularized tissues to harmful stimuli such as infectious agents, mechanical damage, chemical irritants, etc. Inflammation has both local and systemic manifestations and may be either acute or chronic.

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2
Q

is inflammation protective?

A

Yes.
Protective response intended to eliminate the initial cause of cell injury and the necrotic cells and tissues arising from the injury
- May be harmful

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3
Q

Inflammation is intimately associated with the repair process. True/False

A

True

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4
Q

what are the objectives of inflammation?

A
  • Localize and eliminate the causative agent
  • Limit tissue injury
  • Begin the process of healing
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5
Q

what are the causes of inflammation?

A
  • Infectious agents
  • Physical agents
  • Chemical agents
  • Immune reactions
  • Necrotic tissue
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6
Q

describe acute inflammation

A

Acute inflammation is an immediate response to a pathogenic factor (e.g., trauma or infection) and has the following features:
Rapid onset (occurs minutes to hours after an encounter with a causative factor)
Transient and typically short-lasting (provided it is not caused by an immunological condition)
Involves the innate immune system
Characterized by five classic signs of inflammation, which are caused by the release of inflammatory mediators

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7
Q

what are the 5 classic signs of inflammation?

A

The five classic signs of acute local inflammation are redness (rubor), swelling (tumor), heat (calor), pain (dolor), and loss of function (functio laesa).

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8
Q

define chronic inflammation

A
  • Chronic local inflammation is due to nondegradable pathogens, prolonged exposure to toxic pathogens, or autoimmune reactions.
  • Cells involved: mononuclear cells (monocytes, macrophages, lymphocytes, plasma cells), fibroblasts
  • Leads to necrosis and fibrosis (simultaneous destruction and formation of new tissue)
  • May last for months to years
  • The mechanism involves two ways of activating macrophages
    1) Classical (proinflammatory): mediated by Th1 cells secreting IFN-γ
    2) Alternative (anti-inflammatory): mediated by Th2 cells secreting IL-4 and IL-13
  • Outcomes
    1) Scarring
    2) Amyloidosis
    3) Neoplasia (e.g., chronic HCV infection → chronic hepatitis → hepatocellular carcinoma)
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9
Q

what are the outcomes of chronic inflammation?

A

1) Scarring
2) Amyloidosis
3) Neoplasia (e.g., chronic HCV infection → chronic hepatitis → hepatocellular carcinoma)

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10
Q

2 ways of macrophage activation during chronic inflammation?

A

1) Classical (proinflammatory): mediated by Th1 cells secreting IFN-γ
2) Alternative (anti-inflammatory): mediated by Th2 cells secreting IL-4 and IL-13

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11
Q

what cells are involved in chronic inflammation?

A

mononuclear cells (monocytes, macrophages, lymphocytes, plasma cells), fibroblasts

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12
Q

what is the aim of acute inflammation?

A

The aim is to get the neutrophils to the site of injury as fast as possible to eliminate pathogen or clear necrotic debris

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13
Q

what are the components of acute inflammation?

A
  1. Vasodilatation
  2. Endothelial permeability
  3. Extravasation of neutrophils
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14
Q

what are the 2 major events of acute inflammation?

A

vascular and cellular response

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15
Q

describe vascular and cellular response of acute inflammation

A

vascular response: vasodialtion and icnreased vascular permeability
cellular response:extravasation of neutrophils

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16
Q

what are the sequence of events of acute inflammation?

A

1) local hemodynamic changes (vasoconstriction → vasodilation)
2) Increase in vascular permeability
3) Extravasation of leukocytes
4) Phagocytosis and killing of the phagocytosed pathogen or lysis of the phagocytosed particles
5) Outcome of inflammatory response

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17
Q

what is the reason of pain seen with acute inflammation?

A

Stimulation of free nerve endings by certain mediators and H+
Prolonged stimulation → sensitization of ion channels (e.g., TRPV1) → hyperalgesia

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18
Q

what are the mediators of pain seen with acute inflammation?

A

Bradykinin

PGE2

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19
Q

what is the reason for swelling seen with acute inflammation

A

Release of mediators from immune cells and endothelium or damage to endothelium → separation of endothelial junctions → separation of endothelial cells → ↑ vascular permeability and ↑ paracellular movement of fluid → leakage of protein-rich fluid to the interstitial tissue → ↑ oncotic tissue in the interstitium → accumulation of fluid in the interstitium

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20
Q

what are the mediators for swelling seen with acute inflammation

A

Histamine
Leukotrienes (C4, D4, T4)
Serotonin

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21
Q

what is the mechanism of heat and redness seen with acute inflammation?

A

Release of vasoactive mediators by immune cells and endothelium → vasodilation → ↑ blood flow

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22
Q

what are the mediators of heat and redness?

A

Histamine
Bradykinin
Prostaglandins (PGE2, PGD2, and PGF2)
NO

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23
Q

describe the vascular event of acute inflammation?

A
  • Vasoconstriction- transient (few seconds)
  • Vasodilatation
  • Increased vascular permeabilityà exudation of protein-rich fluid
  • loss of fluidà concentration of red cells and increased viscosityà blood stasis
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24
Q

what are the sources of mediators released during acute inflammation?

A

1) Histamine—Basophils, platelets, mast cells
2) Serotonin–Platelets
3) Prostaglandins (PGE2, PGD2, and PGF2)–Leukocytes, platelets, endothelial cells
4) Bradykinin –Plasma
5) NO–Endothelial cells

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25
Q

what is the reason for increased vascular permeability?

A 
•Increased hydrostatic pressure
•decrease in intravascular osmotic pressure
•Changes in endothelial cells
   -Endothelial cell contraction
   -Junctional retraction
   -Endothelial injury
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26
Q

how endothelial cell contraction occur?

A

Due to the action of inflammatory mediators (histamine, serotonin, bradykinin, leukotrienes C4, D4, and T4)
Occurs rapidly and does not last long
Results in the opening of interendothelial spaces and paracellular leakage of plasma

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27
Q

during acute inflammation, hydrostatic pressure decrease inside the vessel. True/False

A

False.

Vasodilatationà increased blood flowà increased hydrostatic pressure

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28
Q

increase hydrostatic pressure result in the development of exudate or transudate?

A

transduate-ultrafiltrate blood plasma (contains little protein

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29
Q

what happens with osmotic pressure inside the vessel during acute inflammation?

A

it decreases due to loss of protein-rich fluid, whereas osmotic pressure in interstitial tissue increases.

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30
Q

exudate or transudate is the characteristic fluid of acute inflammation?

A

exudate (protein-rich fluid) due to Leads to leakage of plasma content into the interstitial tissue

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31
Q

compare exudate and transudate

A 
1)Transudate
Extravascular fluid with low protein concentration
Specific gravity < 1.012
Hydrostatic imbalance
2)Exudate
Extravascular fluid with high protein concentration and cellular debris
Specific gravity > 1.020
Alteration in vascular permeability
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32
Q

alteration in vascular permeability result in transudate formation. True/False

A

False.

Leakage of protein-rich fluid through pores of the vessel–exudate

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33
Q

describe the cellular response of acute inflammation

A

Within inflamed tissue, leukocytes (mainly neutrophils in early infection) interact with the vascular endothelium and leave the blood vessels to migrate to the site of infection. The process of neutrophil extravasation from the blood to the inflamed tissue occurs in 5 steps:

  • margination
  • rolling
  • adhesion
  • diapedesis
  • migration.
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34
Q

what are the main effector cells of acute inflammation

1) macrophages
2) neutrophils
3) lymphocytes
4) NK cells

A

neutrophils

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35
Q

describe the margination

A
  • Leucocytes moving from the centre of the vessel towards the periphery
  • Normal flow - RBC’s and WBC’s flow in the centre of the vessel
  • A cell poor plasma is flowing adjacent to endothelium
    As blood flow slows, WBC’s collect along the endothelium à Margination
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36
Q

what are the 2 mechanisms of margination?

A

The two main mechanisms that allow for margination are rouleaux formation and dilation of post-capillary venules

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37
Q

what is rouleaux formation?

A

An aggregation of erythrocytes with the appearance of a stack of coins on peripheral blood smear. This aggregation is caused by increased concentrations of plasma proteins (e.g., fibrinogen, immunoglobulins).
The liver releases increased amounts of fibrinogen (an acute-phase protein) in response to cytokines released by macrophages, monocytes, and other cells near the site of inflammation.
Increased fibrinogen → rouleaux formation → neutrophils are pushed against endothelium of the venules

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38
Q

what is endothelial activation?

A

The underlying stimulus causes a release of mediators which activate the endothelium causing selectins and other mediators to be moved quickly to the surface

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39
Q

describe rolling

A
  • Neutrophils bounce or roll along with the endothelial cells
  • Transiently adhere to endothelial cells
  • mediated by selectins molecules (transiently bind to their receptors)
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40
Q

rolling is mediated by what molecules?

A

1)On endothelial cells
–P-selectin: stored and released from Weibel-Palade bodies within the endothelium in response to inflammation
Release is mediated by histamine.
–E-selectin: released in response to inflammatory mediators, such as TNF and IL-1
–Other: GlyCAM-1, CD34
2)On leukocytes
-Neutrophils and other leukocytes express Sialyl-LewisX and L-selectin, respectively.
These molecules transiently bind to and dissociate from endothelial selectins, allowing leukocytes to roll along the vascular wall

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41
Q

describe adhesion

A

Leukocytes firmly adhere to endothelial cells

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42
Q

leukocyte adhesion is mediated by…

A

by integrins, ICAM-1 and VCAM-1.

1) On endothelial cells
- -Intercellular adhesion molecule (ICAM, also called CD54)
- -Vascular adhesion molecule (VCAM, also called CD106)
- -Both upregulated by TNF and IL-1
2) On neutrophils and lymphocytes
- -Neutrophils: β2-integrin (lymphocyte function-associated antigen-1, LFA-1, composed of CD18 and CD11a) → binds to ICAM
- -Lymphocytes and monocytes: β1-integrin → binds to VCAM
- -Expression of integrins is activated by leukotriene B4 (LTB4) and C5a

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43
Q

what is transmigration (diapedesis?)

A

Movement of leukocytes through the blood vessel wall to the interstitium
Neutrophils release type IV collagenase, which dissolves the basement membrane and allows them to exit the interstitial space.

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44
Q

transmigration is mediated by?

A

Requires expression of platelet endothelial cell adhesion molecule-1 (PECAM-1, also called CD31) on neutrophils, endothelial cells, and platelets

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45
Q

what is chemotaxis (migration)?

A

The process by which leukocytes move to the cite of inflammation after leaving the blood vessels

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46
Q

list common chemoattractants

A
  • Leukotrienes: e.g., LTB4
  • Platelet-activating factor (PAF)
  • Chemokines: e.g., IL-8
  • Kallikrein
  • Complement fragments: e.g., C5a
  • Bacterial products
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47
Q

what are toll-like receptors? (TLR)

A

Pattern recognition receptors that bind to pathogen-associated molecular patterns (PAMPs)
Activate the NF-κB pathway

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48
Q

what is opsonization?

A

A process by which pathogens and immune complexes are marked with an opsonin (e.g., complement factor C3b) for phagocytosis, after which the pathogen can be eliminated by phagocytes that express opsonin receptors, e.g., Fc receptor and complement receptor 1.

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49
Q

what are the common opsonins?

A

C3b

immunoglobulins

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50
Q

what is the phagocytosis?

A

Phagocytosis is the process by which foreign particles, cell debris, or microbes are engulfed and degraded. Cells capable of phagocytosis are called phagocytes (e.g., neutrophils, macrophages). Phagocytosis involves 3 sequential steps: recognition of a target, engulfment, and degradation or killing of the engulfed particle.

1) Recognition
2) engulfment
2) killing

51
Q

rolling vs adhesion

A

mediated by selectins vs cellular adhesion molecules (CAM) (weak vs strong adhesion)

52
Q

selectins bind to?

A

Sialyl-LewisX on the cell surface

53
Q

CAMs bind to?

A

Integrins on leukocytes
Eg. Alpha-B2 heterodimers:
• LFA-1and Mac-1 bind to ICAM-1
• VLA-4 binds to VCAM-1

54
Q

expression of P selectin on endothelium is activated by?

A

histamine

55
Q

expression of E selectin on endothelium is activated by?

A

TNF, IL-1

56
Q

CAMs are upregulated by?

A

TNF, IL-1

57
Q

β1-integrin vs β2-integrin

A

bind to VCAM vs ICAM

58
Q

expression of integrins is activated by?

A

leukotriene B4 (LTB4) and C5a

59
Q

where transmigration commonly occur?

A

at post-capillary venule

60
Q

how acute inflammation is terminated?

A

inflammation declines due to mediators only being produced transiently (have short half-lives). It is also regulated by stop signals that are activated, such as:

  • switch from proinflammatory arachidonate metabolites (LTs) to anti-inflammatory forms (lipoxins)
  • production of anti-inflammatory cytokines such as TGF-B and IL-10.
  • neural impulses that inhibit macrophage TNF production
61
Q

which are the anti-inflammatory cytokines?

A

L-10

TGF-β

62
Q

what substance switch from proinflammatory arachidonate metabolites (LTs) to anti-inflammatory forms

A

lipoxins (LXA4 and LXB4)

63
Q

a difference of cell vs plasma-derived chemical mediators of inflammation?

A

A.Plasma-derived
–Typically made in the liver
–Circulate as inactive precursors
–Activated by proteolysis
B. Cell-derived
– Preformed and released by granular exocytosis (Sequestered intracellularly) leading to immediate activity
– Synthesized de novo following a stimulus

64
Q

give examples of chemical mediators of inflammation

A
  • Vasoactive amine
  • Plasma proteases
  • Phospholipid-derived products
  • Cytokines
  • Nitric oxide
  • Lysosomal enzymes
  • Oxygen derived free radicals
65
Q

describe histamine?

A
  • Vascular dilatation and leakage
  • Found in mast cells, basophils, and platelets
  • Released in response to stimuli
  • Promotes arteriolar dilation and venular endothelial contraction
66
Q

list cells containing histamine

A

Found in mast cells, basophils, and platelets

67
Q

what are the function of histamine?

A
  • Vascular dilatation and leakage
  • Promotes arteriolar dilation and venular endothelial contraction
  • Results in a widening of interendothelial cell junctions with increased vascular permeability (a contraction of endothelial cells)
68
Q

describe serotonin

A
  • Vascular dilatation and leakage
  • Vasoactive effects similar to histamine
  • Found in platelets
  • Released when platelets aggregate
69
Q

serotonin is found in?

A

platelets, also synapse

70
Q

what are the effects of serotonin?

A

Vascular dilatation and leakage

71
Q

serotonin promote platetet aggregation. True/False

A

True

72
Q

what are the plasma proteases involved in acute inflammation?

A
  • Complement system
  • Kinin system
  • Clotting system
73
Q

what are the phospholipid-derived products involved in acute inflammation?

A
  • Arachidonic acid metabolites

- Platelet-activating factor (PAF)

74
Q

what is PAF?

A

A pro-inflammatory cytokine produced by various cells of the immune system such as neutrophils, monocytes, and macrophages. Involved in platelet aggregation and the development of septic shock and bronchoconstriction.

  • Induces aggregation of platelets
  • Causes vasoconstriction and bronchoconstriction
  • Enhances leukocyte adhesion, chemotaxis, degranulation
75
Q

describe cytokines

A
  • Short-acting soluble mediators
  • Produced by many cell types
  • Multifunctional
  • Systemic effects
76
Q

list proinflammatory cytokines

A 
Proinflammatory cytokines (Th1 cytokines): stimulate the immune system
Interleukins 1, 6, 8, 12, 18, IFN-γ, and tumor necrosis factor
Induce fever, inflammation, and tissue destruction in response to infection, injury, or ischemia
Uncontrolled action is deleterious and can lead to multiorgan dysfunction
77
Q

list anti-inflammatory cytokines

A

Anti-inflammatory cytokines (Th2 cytokines): suppress the immune system
Interleukins 4,10, 11,13, TGFβ
Suppress proinflammatory cytokine secretion and inhibit binding of proinflammatory cytokines to their receptors
An imbalance between the pro-inflammatory and anti-inflammatory cytokine response is responsible for several immune-mediated diseases (e.g., rheumatoid arthritis, inflammatory bowel disease, multiple sclerosis).

78
Q

what is the role of NO

A
  • Toxic to bacteria
  • Vasodilatation
  • Tissue damage
79
Q

NO is vasodilatory of vasoconstrictive?

A

vasodilation

80
Q

what is the main enzyme of the lysosome?

A

The main enzyme stored in lysosomes is acidic phosphatase!

81
Q

arachidonic acid is derived from?

A

cell membrane phospholipids

82
Q

what is the role of phospholipase A2

A

release arachidonic acid from the cell membrane

83
Q

what metabolites derived from arachidonic acid are involved in acute inflammation?

A

prostaglandins and leukotrienes

84
Q

what cells produce prostaglandins?

A

mast cells, macrophages, endothelial cells and platelets.

85
Q

which enzymes are involved in the production of prostaglandins from arachidonic acid?

A

cyclooxygenases (COX1 and 2)

86
Q

what is the role of PGE2?

A

fever

87
Q

what is the role of PGD2/I2/E2?

A

vasodilation and permeability

88
Q

what is thromboxane A2

A

An arachidonic acid derivative and potent platelet aggregator and vasoconstrictor. Inhibition of thromboxane A2 synthesis in thrombocytes is responsible for aspirin’s antiplatelet effect.
Platelets contain thromboxane synthase

89
Q

describe prostacyclin (PGI2)

A

A lipid-derived compound that stimulates vasodilation by inducing smooth muscle relaxation. It also inhibits platelet aggregation.

90
Q

what are the role of leukotrienes?

A

A group of inflammatory mediators produced by leukocytes that potentiate allergic and asthmatic responses. They are metabolites of arachidonic acid and are produced by the enzyme 5-lipoxygenase.

91
Q

leukotrienes vs prostaglandins?

A

synthesized from arachidonic acid by cyclooxygenase vs lipooxygenase

92
Q

which leukotriene attracts and activates neutrophils?

A

LTB4

93
Q

which leukotrienes cause vasospasm, bronchospasm, and increased permeability

A

LTC4,LTD4 andLTE4

94
Q

PGI2, PGE1, PHE2, PGD2 vs LTC4/D4/E4, TXA2

A

vasodilation vs vasoconstriction

95
Q

what LTs increase vascular permeability?

A

LTC4/D4/E4

96
Q

which LT is involved in chemotaxis?

A

LTB4

97
Q

describe the complement system

A

A group of proteins that circulate in the blood as inactive precursors. After stimulation by antibody complexes (classical pathway) or by pathogens (alternative pathway), complement proteases can activate other complement precursors, which leads to a cascade of reactions that enhances the function of antibodies and phagocytes.

98
Q

describe the classical pathway of complement activation

A

Classical pathway: activated by IgM or IgG complexes binding to the pathogen (via C1)

99
Q

describe the alternative pathway of complement activation

A

Alternative pathway: activated directly by pathogen rather than by antigen-antibody complexes (via C3)

100
Q

does the alternative complement activation pathway require antibodies?

A

no

Does does not require antibody to activate

101
Q

which complement product is involved in opsonization/

A

C3b

102
Q

what is the role of complement C5-9

A

C5–C9 form the membrane attack complex (MAC) → perforation of the cell wall → cell lysis

103
Q

what complement products are involved in mast cell and granulocyte activation causing anaphylaxis?

A

C3/C4/C5

104
Q

which complement product is involved in chemotaxis of neutrophils

A

C5a

105
Q

which complement product is involved in the clearance of immune-complexes

A

C3b

106
Q

describe kinin cascade

A
  • Leads to the formation of Bradykinin
  • Bradykinin causes
    1) Increased vascular permeability
    2) Arteriolar dilatation
    3) Smooth muscle contraction
    4) Pain
  • Bradykinin is short-lived (kininases)
107
Q

what are the functions of bradykinin?

A

1) Increased vascular permeability
2) Arteriolar dilatation
3) Smooth muscle contraction-bronchoconstriction

108
Q

what is the key to the activation of the intrinsic pathway of the clotting system?

A

XII (Hageman factor)

The end result is fibrin

109
Q

anti-inflammatory agents act on what pathway of acute inflammation?

A

Arachidonic Acid pathway:
o Aspirin and Non-Steroidal Anti-inflammatory Drugs (NSAID’s) – Cyclooxygenase inhibitors (COX)
o Steroids act, in part, by inhibiting Phospholipase A2

110
Q

what are the mediators of vasodilation?

A 
o	Vasoactive amines
o	Prostaglandins
o	Bradykinin
o	Complement (C3a and C5a)
o	NO
111
Q

what are the mediators that increase vascular permeability? (causing swelling)

A 
o	Vasoactive amines
o	Tissue damage
o	Complement
o	Leucotrienes
o	PAF
o	Bradykinin
112
Q

what are the mediators of chemotaxis?

A

o Complement (C5a)
o Leukotrienes
o Cytokines
o Bacterial products

113
Q

during acute inflammation tissue damage is caused by what?

A

o Lysosomal enzymes
o Oxygen metabolites
o Nitric oxide

114
Q

what is the pathophysiology of fever?

A

Pyrogens are substances that cause fever. Exogenous pyrogens are usually microbes or their products. The best-studied are the lipopolysaccharides of gram-negative bacteria (commonly called endotoxins) and Staphylococcus aureus toxin, which causes toxic shock syndrome. Fever is the result of exogenous pyrogens that induce the release of endogenous pyrogens, such as interleukin-1 (IL-1), tumor necrosis factor-alpha (TNF-alpha), IL-6 and other cytokines, which then trigger cytokine receptors in the hypothalamus, increasing COX activity on perivascular cells of hypothalamus and producing PGE2
Prostaglandin E2 synthesis appears to play a critical role., in the hypothalamus, it increases the set point of body temperature,

115
Q

what are the beneficial effects of inflammation?

A 
o	Dilution of toxins
o	Arrival of antibodies to the site of inflammation
o	Drug transport
o	Delivery of nutrients and oxygen 
o	Fibrinogen----Fibrin (delays bacterial spread)
o	Destruction of the microbial agent 
o	Removal of tissue debris
o	Stimulation of immune response
116
Q

inflammation contribute to drug delivery.true/False

A

True (increase blood flow, increase vessel permability)

117
Q

what are the harmful effects of inflammation?

A

o Mechanical effect e.g., epiglottitis
o Impaired flow e.g., acute meningitis
o Impaired function
o Tissue destruction

118
Q

what are the outcomes of acute inflammation?

A

1) Resolution with regeneration
2) Resolution with scarring (healing and repair)
3) abscess formation
4) chronic inflammation

119
Q

describe resolution with regeneration outcome of the acute inflammation

A
  • Cellular debris and pathogens are removed by macrophages.
  • Edema is resorbed via lymphatic vessels.
  • Damaged tissue is repaired via the proliferation of stem cells.
120
Q

celular debris after acute inflammation is removed via

1) macrophages
2) neutrophils

A

macrophages

121
Q

describe resolution with scarring (healing and repair) outcome of the acute inflammation

A
  • Cellular debris, pathogens, and edema are cleared.
  • There is a lack of stem cells to replace the damaged tissues → Original tissue is replaced by fibrotic scar tissue.
    1. after substantial tissue destruction
    2. setting of abundant fibrin exudation (organization)
122
Q

describe the abscess formation outcome of the acute inflammation

A

Inflammation → pus formation and tissue necrosis

The focus of necrosis is separated from healthy tissues by a fibrous capsule.

123
Q

describe the progression to chronic inflammation outcome of the acute inflammation

A

Persistence of causative factor → antigen presentation to T-helper cells → activation of CD4+ Th cells → infiltration of affected tissues

General Pathology (9 decks)

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