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MOD Exam 1 > Inflammation and Repair > Flashcards

Inflammation and Repair Flashcards

1
Q

Eosinophils are abundant in what types of reactions?

A

Those mediated by IgE

Parasitic infections

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2
Q

The increase in vascular permeability is seen in what type of vasculature?

A

postcapillary venules!!

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3
Q

Which of the cyclooxygenase enzymes are present in both normal tissues and in response to inflammatory stimuli?

A

COX-1

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4
Q

What do M2 macrophages produce that assist in tissue repair?

A

Growth factors

TGF-β

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5
Q

5-lipoxygenase generates what lipid mediator?

A

Leukotrienes

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6
Q

What cells are the most important in inflammatory reactions?

A

cells that phagocytose: macrophages and neutrophils

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7
Q

Overall function of the leukotriene mediators?

A

Increased vascular permeability, chemotaxis, leukocyte adhesion and activation

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8
Q

Why is pus considered an exudate?

A

it contains leukocytes (mainly neutrophils), cellular debris and microbes

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9
Q

Keloid scar formation is more common in what population of individuals?

A

African Americans

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10
Q

What prostaglandin is responsible for pathogeneis of pain and fever during inflammatory response?

A

PGE2

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11
Q

inflammation associated with cytokine-induced systemic reactions are referred to as?

A

acute-phase response

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12
Q

What type of macrophage arises from the classical pathway of activation?

What cytokines are involved?

A

An M1 macrophage

microbes, INF-γ

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13
Q

What type of macrophage arises from the alternative pathway?

What cytokines are involved?

A

M2 macrophage

IL-13 and IL-4

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14
Q

What other mediator has actions similar to histamine, with the function of increasing vascular permeability, contraction of smooth muscle, dilation of blood vessels and pain when injected into the skin?

A

Bradykinin

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15
Q

In granulomas, what contributes to the formation of the central zone of necrosis?

A

Hypoxia and free-radical mediate injury

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16
Q

Liver macrophages

A

Kupffer cells

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17
Q

Deficiency in C1 inhibitor leads to what condition?

A

Hereditary angioedema

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18
Q

What other function does C5a have, besides stimulation of histamine release?

A

C5a is a chemotatic agent

C5a also activates the lipoxygenase pathway, causing further release of inflammatory mediators

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19
Q

What leukocyte prodominates in the first 24 hours of inflammation?

A

Neutrophils

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20
Q

What is the complement system?

A

A collection of soluble proteins and membrane receptors that function in host defence against microbes and pathologic inflammatory rxns

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21
Q

Leukocytosis is typically induced by what sort of infections?

A

Bacterial

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22
Q

TH17 cells secrete what cytokine and what is its function?

A

IL-17

induce the secretion of chemokines responsible for recruiting neutrophils and monocytes to the site of inflammation

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23
Q

What lymphocyte secretes cytokine and thus promotes inflammation?

A

CD4+ T-cells

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24
Q

The cytokines responsible for leukocyte adhesion and migration are?

A

TNF and IL-1

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25
Q

Acute inflammation occurs in response to what circumstances?

A

Infection, necrosis

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26
Q

Immune response cells involved in chronic arthritis?

A

lymphocytes, macrophages

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27
Q

If fibrosis occurs in a space occupied by an exudate it is termed

A

Organization

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28
Q

The M1 macrophage produce what mediators that contribute to inflammation?

A

IL-1, IL-12, IL-23 and chemokines

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29
Q

What cells produce the mediators of CT deposition?

A

Primarily M2 macrophages; mast cells and lymphocytes may be present and produce them as well

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30
Q

Why is aspirin used to bring down fevers?

A

ASA inhibits cyclooxygenase, therefore preventing the production of prostaglandins

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31
Q

what other molecules are generated from arachidonic acid by lipoxygenase, but function as anti-inflammatory agents?

A

Lipoxins (LXA4 and LXB4)

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32
Q

What anti-inflammatory mediators are involved in termination of the acute inflammatory response?

A

TGF-β and IL-10

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33
Q

What pathway ensures that new blood vessels have proper spacing to effectively supply healing tissue with blood?

A

Notch signaling pathway

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34
Q

What is the mechanism behind leukocyte-dependent tissue injury?

A

When a leukocyte is activated, their effector mechanisms do not distinguish between host and offender, leading to damage of normal cells and tissues in addition to a microbe

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35
Q

Why do macrophage mannose binding receptors only bind microbes and not host cells?

A

These receptors bind terminal mannose and fructose residues of microbial glycoproteins and glycolipids rather than terminal sialic acid or N-acetylgalactosamine

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36
Q

What are the cardinal signs of inflammation?

A

Rubor (redness)

Tumor (swelling)

Calor (warmth)

Dolor (pain)

Functio laesa (loss of function)

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37
Q

What is the downside to using TNF antagonists as a treatment for chronic inflammatory diseases?

A

Patients become more susceptible to mycobacterial infections, with a reduced ability to kill intracellular microbes

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38
Q

Degradation of collagen and other ECM components involved in deposition of connective tissue is accomplished by what enzymes?

What do these enzymes depend on for their activity?

A

Matrix metalloproteinases (MMPs)

Metal ions

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39
Q

Wound dehiscence and ulcerations occur as a result of

A

inadequate formation of a scar or granulation tissue

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40
Q

Components of exudate?

A

Extravascular fluid with high protein concentration and cellular debris

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41
Q

What is the primary response cell in pseudomonas bacterial infections?

A

Neutrophils

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42
Q

Acute inflammatory reactions have 3 possible outcomes:

A
  1. Complete resolution
  2. healing by CT replacement (scarring)
  3. Progression to chronic inflammation
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43
Q

Of the factors that influence tissue repair, what is the most common systemic cause of abnormal wound healing

A

Diabetes Mellitus

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44
Q

Under what circumstances would a wound heal by first intention?

A

When the injury involves only the epithelial layer

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45
Q

Lung macrophages

A

alveolar macrophages

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46
Q

Antagonists to what cytokine have been shown to be an effective tx for chronic inflammatory diseases?

A

TNF

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47
Q

What are the types of selectins that are involved in leukocyte rolling?

A

L-selectin on leukocytes

E-selectin on endothelium

P-selectin on platelets and endothelium

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48
Q

What are the three pathways of complement?

A

Classic pathway

Alternative pathway

Lectin pathway

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49
Q

Immune cells involved in pulmonary fibrosis?

A

macrophages and fibroblasts

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50
Q

Which of the neutrophil granule types contains myeloperoxidase?

A

Azurophilic granules

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51
Q

Of the factors the influence tissue repair, which is the most clinically important delay of healing?

A

infection

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52
Q

What drives the regeneration of tissues and injured cells?

A

Growth factors

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53
Q

What is the result of vasodilation?

A

Increased blood flow, leading to erythema at the site of infection

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54
Q

Lymphangitis

A

Inflammation of the lymphatics, often leaves a red streak to the site of lymph nodes as the lymph fluid brings infection with it.

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55
Q

Repair begins 24 hours after injury with the emigration and induction of proliferation of what cell types?

A

fibroblasts and endothelial cells

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56
Q

The selectin ligands are what type of molecules?

A

sialylated oligosaccharides bound to mucin-like glycoprotein backbones

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57
Q

Steps involved in deposition of CT

A

Migration and proliferation of fibroblasts to site of injury

Deposition of ECM proteins produced by fibroblasts

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58
Q

Overall action of prostaglandins?

A

Vasodilation, pain, fever

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59
Q

What effects does hepcidin have during the acute-phase reaction?

A

Elevated levels of hepcidin reduce the availability of iron, leading to the anemia often seen with chronic inflammation

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60
Q

Normal differental count of eosinophils in WBC count?

A

1-4%

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61
Q

During the growth factor phase of liver regneration, cells release what GFs to act on hepatocytes, triggering them to move from G0 phase into the G1 phase of the cell cycle?

A

HGF and TGF-α

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62
Q

What are the important mediators of the acute-phase response

A

IL-1

TNF

IL-6

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63
Q

What is the most common mechanism of vascular leakage and what mediators elicit this response?

A

contraction of endothelial cells leading to an increase in space of the tight junctions

mediated by histamine, bradykinin, and leukotrienes

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64
Q

TNF causes what pathologic effects in the heart?

A

decreased cardiac output

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65
Q

Under what circumstances would a wound heal by second intention?

A

when cell or tissue loss is more extensive, as seen in large wounds, abscesses, ulcerations and ischemic necrosis

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66
Q

What is the most common cause of chronic inflammation?

A

Persistent infection that cannot be cleared by an acute inflammatory response

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67
Q

What is typically used to treat autoinflammatory syndromes?

A

IL-1 antagonists

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68
Q

LTC4, LTD4, and LTE4 are cysteinyl-containing leukotrienes that are responsible for?

A

Causing intense vasoconstriction, bronchospasms, and increased permeability of the venules

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69
Q

C3b is an opsonin, what is the purpose of an opsonin?

A

Opsonins promote phagocytosis by making the microbe “tastier” to phagocytes

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70
Q

Acute inflammation has three major components:

A
  1. dilation of small blood vessels to increase blood flow
  2. Increased permeability of vasculature to allow for plasma proteins and leukocytes to leave circulation
  3. Migration of the leukocytes to site of injury
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71
Q

Activation of complement is controlled by which regulatory proteins?

A

C1 inhibitor

Decay accelerating factor

CD59

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72
Q

The presence of transudate indicates what?

A

There has been an osmotic or hydrostatic imbalance across a vessel wall without an increase in permeability

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73
Q

Tissue repair via regeneration occurs how?

A

Proliferation of residual cells

Maturation of stem cells

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74
Q

What is the main response cell in viral infections?

A

Lymphocytes

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75
Q

Function of M2 macrophages

A

Tissue repair

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76
Q

Normal differental count of neutrophils in WBC count?

A

40-70%

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77
Q

What happens when an infection causes an inflammatory response that is systemic, rather than local, causing widespread pathologic abnormalities?

A

Sepsis

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78
Q

When does fibrinous inflammation develop?

A

When vascular permeability allows large molecules like fibrin to pass out of the blood

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79
Q

As stasis develops, what do blood leukocytes do?

A

They accumulate along the vascular endothelium to then eventually migrate through and out to the tissues.

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80
Q

in the process of NET formation, neutrophils lose their nuclei, ultimately lead to

A

death of the neutrophil

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81
Q

Granulomatous inflammation is a form of chronic inflammation characterized by

A

collections of activated macrophages, often with T-lymphocytes and sometimes associated with a central region of necrosis

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82
Q

How do giant cells form?

What cytokine induces the formation?

A

Fusion of multiple activated macrophages

INF-γ

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83
Q

What is characteristic of an immune granuloma?

A

They care caused by agents that induce a persistent T-cell mediated immune response

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84
Q

What event follows vasodilation in an acute inflammatory response

A

increased permeability of the mnicrovasculature, leading to leakage of protein-rich fluid into extravascular tissue (exudate)

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85
Q

Mediators of acute inflammation include:

A

Toll-like receptors

Arachadonic acid metabolites

Mast cells

Complement

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86
Q

Angiogenesis is the process of developing new blood vessels and is critical in healing, these new vessels are leaky d/t the effects of what growth factor?

A

Vascular endothelial growth factor (VGEF)

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87
Q

Principal mediators of vasodilation?

A

Histamine

Prostaglandins

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88
Q

Hematopoietic cells, surface epithelium, columnar epithelium of the GI tract, uterus and uterine tubes, transitional epithelium of the urinary tract are considered to be labile tissues because of what characteristic?

A

They are continuously being lost and replaced by the maturation of tissue stem cells and proliferation of mature cells.

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89
Q

What enzyme is responsible for creating superoxide anion during the respiratory burst?

A

NADPH oxidase

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90
Q

What circulating protein recognizes microbial sugars and activates the complement system in order to produce mediators of inflammation?

A

Mannose-binding lectin

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91
Q

TH2 cells produce what cytokines and what are their functions?

A

IL-4, IL-5, IL-13

Recruit and activate eosinophils, promote class switching to IgE, activation of M2 macrophages

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92
Q

Through what types of reactions does tissue repair occur?

A

Regeneration

Deposition of CT to form a scar

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93
Q

What leukotriene is a potent chemotactic agent for neutrophils?

A

LTB4

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94
Q

Elevated levels of CRP in serum can be indicative of?

A

increased risk of MI

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95
Q

Principal mediators of increased vascular permeability

A

Histamine

5HT

C3a and C5a

LTC4, LTD4, LTE4

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96
Q

what are the major participants in an inflammatory reaction?

A

blood vessels and leukocytes

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97
Q

Monocytes migrate to various tissues where they then differentiate into macrophages, what two pathways give rise to macrophages?

A

Classical pathway

Alternative pathway

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98
Q

What growth factors are involved in the structural maturation of newly formed blood vessels?

A

Angiopoietin 1 and 2

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99
Q

When would tissue repair by CT deposition occur?

A

When tissues are incapable of completely healing by regeneration

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100
Q

Erythrocyte sedimentary rate (ESR) is often measured to test for an inflammatory response, what is the mechanism behind this?

A

Fibrinogen, an acute-phase protein, binds to RBCs, causing them to form stacks (rouleaux) that sediment more rapidly than an individual RBC

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101
Q

Tissue macrophages, mast cells and endothelial cells that encounter microbes and dead tissue respond by secreting cytokines that induce expression of adhesion molecules, what are these cytokines?

A

TNF (tumor necrosis factor) and IL-1

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102
Q

Leukocytes transmigrate through interendothelial spaces toward the site of infection with the help of what adhesion molecules?

A

CD31 or PECAM-1

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103
Q

Macrophages are tissue cells, when they are circulating in blood they are referred to as?

A

Monocytes

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104
Q

TNF and IL-1 produce what pathologic effect in skeletal M?

A

Increased insulin resistence

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105
Q

What is the function of Decay Accelerating Factor?

A

Prevents the formation of C3 convertase

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106
Q

Steps involved in phagocytosis

A
  1. Recognition and attachment
  2. Engulfment
  3. Killing and degradation
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107
Q

For what reason is tissue destruction a hallmark of chronic inflammation?

A

Certain activities of macrophages promote inflammation and tissue damage

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108
Q

Killing of microbes is accomplished via

A

ROS and NO

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109
Q

What lipid mediator is responsible for vasoconstriction and platelet aggregation

A

Thromboxane A2

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110
Q

For what reasons are neutrophils the predominate responder?

A

There are more of them in the blood, they respond rapidly to chemokines, they attach more firmly to cell adhesion molecules (P and E selectins)

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111
Q

Once a microbe has bound to a phagocytic receptor, it undergoes engulfment. What are the steps?

A

The plasma membrane extends pseudopods around the microbe, forming a vesicle around it (phagosome)

The phagosome then fuses with a lysosome to form a phagolysosome

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112
Q

What is more potent for causing vascular permeability and bronchospasm (histamine or leukotriene)?

A

Leukotrienes

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113
Q

What cytokine is involved in the first priming phase of liver regeneration?

What cells produce this cytokine?

A

IL-6 produced by Kupffer cells

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114
Q

Wound contraction occurs with the help of what cell type?

A

myofibroblasts

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115
Q

Deficiency in DAF and CD59 lead to what disease?

A

Paroxysmal nocturnal hemoglobinuria (PNH)

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116
Q

What causes neutrophilia?

A

A bacterial infection that increases the number of neutrophils in the blood count

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117
Q

How are prostaglandins produced in order to cause an increase in body temperature?

A

Bacterial LPS stimulate leukocytes to release IL-1 and TNF

IL-1 and TNF stimulate cyclooxygenase, which converts arachidonic acid into prostaglandins

118
Q

What is the role of PDGF growth factor in angiogenesis?

A

Recruits smooth muscle cells

119
Q

Exogenous pyrogens involved in the acute phase response

A

LPS, which activates IL-1 and TNF (endogenous pyrogens)

120
Q

What types of phagocytic disorders are considered to be intrinsic?

A

Chronic granulomatous disease

Glycogen storage disease

Chediak-Higashi syndrome

121
Q

How are arachidonic acids released from membrane phospholipids?

A

through the cellular action of phospholipases, specficially phospholipase A2

122
Q

What cytokines are responsible for induction of fever?

A

IL-1 and TNF

123
Q

If a granuloma does not have a central zone of necrosis, what type of granuloma is it?

A

Non-caseating

124
Q

Autoinflammatory syndromes are caused by what type of mutation?

A

Gain of function mutations in the sensors that detect infection

125
Q

What is a common example of purulent inflammation?

A

acute appendicitis

126
Q

Phospholipase A2 is inhibited by __ preventing the production of arachidonic acid

A

Steroids

127
Q

What is the role of TGF-β in angiogenesis?

A

supresses the proliferation and migration of endothelial cells, rather enhancing the ECM protein production

128
Q

M1 macrophages produce what substances that contribute to phagocytosis?

A

ROS, NO, lysosomal enzymes

129
Q

What is the most common exogenous chemotactic substance, attracting leukocytes to the site of inflammation?

A

Bacterial products

130
Q
A
131
Q

What is a leukemoid reaction?

A

Extreme elevations in WBC count (40k-100k) 2/2 infection, similar to counts seen in patients with leukemia

132
Q

In the termination phase of liver regeneration, cells return to G0 phase of the cell cycle with the help of what cytokine?

A

TGF-β

133
Q

Proud flesh results from the formation of excessive amounts of granulation tissue, which often requires removal by cautery or surgical excision.

The exuberant proliferation of fibroblasts that occurs after excision leads to?

A

Formation of desmoids or aggressive firbromatoses

These are low-grade neoplasms (between benign and malignant)

134
Q

The ability of a tissue to repair is determined by what factor?

A

Their intrinsic proliferative capacity

135
Q

What molecules are capable of inhibiting cyclooxygenase and therefor prevent the production of prostaglandins?

A

COX-1 and COx-2 inhibitors, aspirin, indomethacin

136
Q

What mechanisms are in place to protect against oxygen-derived radicals that are released from leukocytes after exposure to microbes?

A

Superoxide dismutase

catalase

glutathione peroxidase

ceruloplasm

transferrin

137
Q

What are the main characteristics of an acute inflammatory response?

A

Edema

Migration of Neutrophils to site of infection

138
Q

Cells primarily invloved in ARDS?

A

Neutrophils

139
Q

Toxic granulations are common in patients with what condition?

A

Sepsis

140
Q

NO is produced by NOS and contributes to microbial killing, of the types of NOS, which does?

A

iNOS (inducible)

141
Q

Inflammatory response cells involved in both acute and chronic asthma?

A

IgE and Eosinophils

142
Q

What causes the decrease in blood flow during an acute inflammatory reaction?

A

The increased permeability and exudation of high protein fluid following vasodilation

143
Q

Parenchymal organs have limited regeneration capabilities except for which organ?

A

Liver

144
Q

What enzyme converts arachadonic acid into leukotrienes?

A

5-Lipoxygenase

145
Q

Cyclooxygenase produces what type of lipid mediator?

What specific subtypes of this enzyme?

A

Prostaglandins

COX-1 and COX-2

146
Q

What is the ligand for the integrin VLA-4?

A

VCAM-1

147
Q

What differentiates chronic inflammation from acute inflammation?

A

Chronic inflammation is a delayed response and is also more specific d/t adaptive immunity

148
Q

What induces a left shift in leukocytosis?

A

the initial accelerated release of cells from the bone marrow caused by TNF and IL-1 leads to an increase in the number of immature neutrophils in the blood

149
Q

What are the major opsonins?

A

IgG, C3b, and mannose-binding lectin

150
Q

What is the predominant lipoxygenase in neutrophils?

A

5-lipoxygenase

151
Q

M1 macrophages produce what factors that contribute to inflammation?

A

IL-1

IL-12

IL-23

Chemokines

152
Q

Since H2O2 is not sufficient in killing microbes, it is converted into hypochlorite using what enzyme?

Where is this enzyme found?

A

Myeloperoxidase (MPO)

Within azurophilic granules of neutrophils

153
Q

What are the hallmarks of chronic inflammation?

A

presence of macrophages, lymphocytes and plasma cells

154
Q

What is the major factor involved in formation of tissue fibrosis?

A

TGF-β

155
Q

Steps involved in angiogenesis:

A
  1. Vasodilation in response to NO and increased permeability of existing blood vessel induced by VGEF
  2. Breakdown of the basement membrane to allow sprouting of new vessel
  3. Migration of endothelial cells to site of injury
  4. Endothelial cell proliferation
  5. Remodeling into capillary tubules
  6. Recruitment of periendothelial cells to form a mature vessel
  7. suppression of endothelial proliferation, migration and deposition
156
Q

Bradykinin is generated via cleavage of Kininogen by what enzyme?

A

Kallikrein

157
Q

In what type of leukocyte are toxic granulations found?

A

Neutrophils

158
Q

what is the most common cause of defective inflammation<

A

Leukocyte deficiency

159
Q

Principal mediators of pain

A

Prostaglandins

Bradykinin

160
Q

what growth factor stimulates the proliferation of hematopoietic stem cells in response to loss of blood cells?

A

Colony-stimulating factor (CSF)

161
Q

What types of phagocytic defects are considered to be extrinsic?

A

abnormalities in opsonization 2/2 deficiencies of Ab and complement factors

162
Q

What lipid mediator is responsible for vasodilation and inhibition of platelet aggregation?

A

Prostacyclin, aka PGI2

163
Q

B and T lymphocytes contribute to chronic inflammation how?

A

They are activated by microbes and other environmental agents, which then amplifies and propagates the chronic inflammatory response

164
Q

what factors influence the outcome of tissue repair?

A

the balance between synthesis and degradation of ECM proteins

165
Q

What is characteristic of foreign body granulomas?

A

They do not elicit an inflammatory or immune response

166
Q

Morphologic patterns of acute inflammation include?

A

Serous inflammation

Fibrinous inflammation

Purulent (suppurative) inflammation

Ulcers

167
Q

What is the purpose of the vascular reactions of acute inflammation?

A

To maxinmize the movement of proteins and leukocytes out of circulation and to the site of injury.

168
Q

Skin macrophages

A

Langerhans cells

169
Q

NETs are produced by what leukocyte?

A

Neutrophil

170
Q

What is the purpose of granuloma formation?

A

Attempt to contain the offending agent that is difficult to eradicate

171
Q

Leukopenia refers to?

A

A decrease in the number of circulating white cells in response to certain infections

172
Q

In what circumstance would a foreign body granuloma form?

A

Sutures, Talc

173
Q

What type of mediators are sequestered in intracellular granules to be released or synthesized de novo?

A

Cell-derived mediators

174
Q

Autoimmune and allergic reactions are often associated with chronic inflammation and are induced by what type of immune cells?

A

Cytokines produced by T lymphocytes

175
Q

What are the sentinel cells that are responsible for producing mediators of acute inflammation?

A

Macrophages

Dendritic cells

Mast cells

176
Q

what molecules are involved in leukocyte rolling and adhesion?

A

Selectins and integrins

177
Q

Normal differental count of monocytes in WBC count?

A

4-8%

178
Q

What growth factor stimulates receptors to induce transcytosis?

A

VEGF: vascular endothelial growth factor

179
Q

What are some examples of diseases with associated granulomatous inflammation?

A

TB

Leprosy

Cat scratch dz

Sarcoidosis

Chrons dz

180
Q

What cells dominate in prolonged inflammatory reactions and why?

A

Monocytes

Have a longer lifespan and can proliferate within tissue

181
Q

What is the cause of septic shock?

A

Severe bacterial infections release large amounts of cytokines (IL-1 and TNF), which leads to disseminated intravascular coagulation, hypotensive shock and metabolic disturbances

182
Q

What is the function of CRP and SAA in the acute phase response?

A

Bind to cell walls and act as opsonins, fix complement, and bind to chromatin

183
Q

When a mediator is triggered by microbes, necrotic tissue, or hypoxia, what happens?

A

Mediators initiate and amplify the inflammatory response; they determine the pattern, severity, and clinical/pathological manifestations of the response

184
Q

What are the types of granulomas?

A

Foreign body

immune

185
Q

There are more than 20 proteins in the complement system, circulating in their ___ form in plasma

A

inactive

186
Q

Arachidonic derived mediators are generated through two enzymes, what are they?

A

cyclooxygenase and 5-lipoxygenase

187
Q

Inflammatory reactions are stimulated by what sort of stimuli?

A

Infections

Tissue necrosis

Foreign bodies

Immune reactions

188
Q

What leads to the formation of a hypertrophic scar? When would this be referred to as a keloid?

A

When there is an accumulation of excessive amounts of collagen localized to the wound

When scar tissue grows beyond its boundaries of the original wound

189
Q

What is one of the earliest manifestations of acute inflammation and what is it mediated by?

A

Vasodilation, mediated by several things but most notably histamine

190
Q

Phagocytic disorders can be divided into two groups based on their defects, what are these groups?

A

Intrinsic

Extrinsic

191
Q

Wound dehiscence occurs most frequently after?

A

abdominal surgery 2/2 increased abdominal pressure

192
Q

Why are eosinophils helpful and why are the damaging?

A

Eosinophils contain granules full of major basic protein, which is toxic to parasites but it causes lysis of mammalian epithelial cells

193
Q

What causes margination of leukocytes?

A

The stasis that occurs in the acute inflammatory response leads to hemodynamic changes that allow for the white cells to assume an peripheral position

194
Q

What inhibits leukotriene C4, D4 and E4 and therefore inhibits bronchospasms?

A

leukotriene receptor antagonists

195
Q

Exogenous pyrogen involved in fever production during the acute phase response

A

LPS

196
Q

What are the NETs made of?

A

a viscous meshwork of nuclear chromtin that binds and concentrates granule proteins

197
Q

Principal mediators in fever

A

IL-1

TNF

Prostaglandins (PGE2 specficially)

198
Q

What is the critical step in complement activation?

A

Cleavage of the C3 component

Can occur via one of three pathways

199
Q

What is the underlying function of mediators of inflammation?

A

inititate and regulate inflammatory response

200
Q

What stimulates the bone marrow to produce leukocytes?

A

IL-1, IL-6 and TNF

201
Q

What type of response is inflammation?

A

A protective response of vascular tissues

202
Q

What is the dominant cell type in most chronic inflammatory reactions?

A

Macrophages

203
Q

What are the steps encountered during a typical inflammatory reaction?

A
  1. The offending agent, located in extravascular tissues, is recognized
  2. Leukocytes and plasma proteins are recruited from circulation to the site of infection
  3. leukocytes and proteins are activated to remove the offending agent
  4. Reaction is controlled (regulated) and terminated
  5. The damaged tissue is repaired
204
Q

Why does acute inflammation have limited specificity?

A

Acute inflammation is an innate immune response

205
Q

What are the morphological hallmarks of acute inflammation?

A

dilation of small blood vessels

accumulation of leukocytes in extravascular tissues, specifically neutrophils

206
Q

What is the function of a neutrophil extracellular trap (NET)?

A

Provide a high concentraion of antimicrobial substances at sites of infection and prevent the spread of infection by trapping them in fibrils

207
Q

What is the function of CD59 in complement regulation?

A

inhibts formation of the membrane attack complex

208
Q

What protein is a chemotactic agent for neutrophils?

A

C5a

209
Q

What would cause a wound to ulcerate?

A

Inadequate vascularization during healing

210
Q

What is the most effective way to destroy phagocytosed material?

A

O2-dependent killing

211
Q

Ulcers commonly form where?

A

In the mucosa of the mouth, stomach, GU tract OR skin and subcutaneous tissue of the LE in older adults/adults with circulatory disturbances (DM)

212
Q

Changes in granulocytes visible in blood smears of patients with inflammatory conditions is known as?

A

Toxic granulations

213
Q

What mediators are responsible for vasodilation and increased vascular permeability of postcapillary venules?

A

PGD2 and PGE2

214
Q

Normal differental count of lymphocytes in WBC count?

A

20-40%

215
Q

What is the effect of macrophages and lymphocytes interacting with one another?

A

Macrophages present Ags to T-cells, which produce cytokines that induce a T-cell response

T-cell cytokines recruit macrophages, promoting more Ag presentation and cytokine secretion

Chronic inflammation is sustained

216
Q

Cell lysis via the MAC complex is the primary pathway for ridding what bacteria?

A

Neisseria

217
Q

What are the most important mediators of acute inflammation?

A

Vasoactive amines

Lipid products (prostaglandins and leukotrienes)

Cytokines

Complement

218
Q

Fluid located in the interstitial tissue or serous cavities, that can be either exudate or transudate is?

A

Edema

219
Q

What is the mechanism behind acute on chronic inflammation?

A

Neutrophils are induced by persistent microbes or mediates produced by activated macrophages and T-lymphocytes

220
Q

When would it be common to see eosinophilia?

A

Allergic reactions

Parasitic infections

221
Q

What are the 3 subsets of CD4+ T-cells

A

TH1

TH2

TH17

222
Q

What enzyme generates the lipoxins, A and B, which function in inhibiting inflammation?

A

12-lipoxygenase

223
Q

Normal differental count of basophils in WBC count?

A

0-1%

224
Q

Immune cells involved in atherosclerosis?

A

macrophages, lymphocytes

225
Q

What type of mediators are produced in the liver and present in their inactive form within circulation?

A

Plasma-derived mediators

226
Q

Morphology of chronic inflammation

A

Infiltration of mononuclear cells (macrophages, lymphocytes, plasma cells)

Tissue destruction

Attempt at healing (angiogenesis, scarring)

227
Q

Efficiency of phagocytosis is ehanced when microbes are

A

opsonized

228
Q

what growth factor is involved in proliferation of endothelial cells?

A

FGF-2

229
Q

What allows for the conversion of low affinity integrins on leukocyes to high affinity integrins in order to promote firm adhesion?

A

Production of TNF and IL-1 at the site of injury followed by expression in high concentrations on the endothelial cells for which leukocytes roll by

230
Q

Acute to chronic transition occurs when?

A

when the acute inflammatory response cannot be resolved d/t persistence of the injurious agent or some interference with the normal processes of healing

231
Q

Resolution of an acute inflammatory reaction involves what?

A

removal of cellular debris and microbes by macrophages, resportion of edematous fluid by the lymphatic system

232
Q

The activation of TLRs leads to upregulation of NF-κB, what effect does this nuclear transcription factor have on inflammation?

A

Activates immune response genes lead to the production of multiple immune mediators

233
Q

An increase in body temperature is caused by what mediator

A

Prostaglandins

234
Q

What process produces the stable fibrous scar?

A

Remodeling of the connective tissue

235
Q

Extensive deposition of collagen in the lungs, liver, kidney and other organs as a result of chronic inflammation is termed?

A

Fibrosis

236
Q

What TLR is located on macrophages and recognizes lipopolysaccharides on the membrane of gram-negative bacteria?

A

CD14

237
Q

Through what mechanism do leukocytes move to the site of infection?

A

Extension of filipodia

238
Q

What cytokines are involved in the systemic acute-phase response, including fever, and are also implicated in sepsis?

A

IL-1, TNF and IL-6

239
Q

The MAC complex functions in cell lysis how?

A

MAC complex inserts into the cell membrane, making the cell more permable to water and ions

240
Q

What lipid mediators are produced from arachidonic acid?

What other name refers to these mediators?

A

Prostaglandins and leukotrienes

Eicosanoids

241
Q

When a granuloma is found, what disease should always be ruled out?

A

Mycobacterium Tuberculosis

242
Q

Steps in scar formation

A
  1. Angiogenesis
  2. Formation of granulation tissue
  3. Remodeling of CT
243
Q

Histological appearance of granulation tissue

A

proliferation of fibroblasts

new blood vessels

Macrophages

244
Q

TNF causes what pathologic effects in blood vessels?

A

Production of thrombus

245
Q

What are the hallmarks of acute inflammation?

A

Presence of neutrophils and edema

246
Q

What will cause lymphocytosis?

A

Viral infections, such as mono, that increase the number of lymphocytes in the blood count

247
Q

What are some examples of non-caseating granulomas?

A

Sarcoidosis, cat scratch disease, chrons disease

248
Q

What cell surface receptor is expressed on mast cells and what ligand binds?

A

FcεRI

bind the Fc region of IgE antibody

249
Q

When an exudate is present, what does this imply?

A

There is an increase in permeability of the vessel endothelium (change in the tight junctions) as a result of tissue injury and an ongoing inflammatory rxn

250
Q

Sensors that activate the inflammasome lead to the production of what cytokine?

A

IL-1

251
Q

Once leukocytes migrate across endothelium, they move to the site of injury via the help of chemoattractants, both endogenous and exogenous, including:

A

Exogenous: bacteria with peptides that posses N-formylmethionine

Endogenous: cytokines (IL-8), complement (C5a), arachadonic metabolites (Leukotriene B4)

252
Q

CNS macrophages

A

Microglia

253
Q

Tissue repair by regeneration is dependent on?

A

The integrity of the ECM

254
Q

C3a and C5a are considered to be anaphylatoxins because of their actions, what is it?

A

Stimulation of histamine release from mast cells, leading to vasodilation and increased vascular permeability

255
Q

A substance that induces fever is referred to as?

A

A pyrogen

256
Q

Where are toll like receptors (TLRs) located and what do they recognize?

A

Cells of the innate immune system ( macrophages and dendritic cells)

They recognize PAMPs located on pathogens

257
Q

Serous inflammation is defined by

A

Exudation of cell poor fluid (transudate) into spaces created by cell injury or into body cavities lined with peritoneum (chest, abd, etc)

258
Q

As blood flows slower, RBCs in small vessels concentrate and the viscosity of blood increases leading to

A

Stasis; the engorgement of small vessels with slow moving RBCs

259
Q

What is a noraml total WBC count?

A

4,000 - 10,000

260
Q

What cells are the source of histamine?

A

Mast cells

Basophils

Platelets

261
Q

Spleen/lymph node macrophages

A

Sinus histiocytes

262
Q

Purulent (suppurative) inflammation is characterized by the production of pus, commonly d/t infection by?

A

Bacteria that cause liquefactive necrosis, such as staphylococci

263
Q

What is critical to the strength of a healing wound site?

A

Collagen synthesis

264
Q

Firm adhesion, which occurs prior to transmigration, is mediated by what cell adhesion molecule?

A

Integrin

265
Q

Factors that influence tissue repair

A

Infection

Diabetes

Nutritional status

Steroids

Mechanical factors

Poor perfusion

Foreign bodies

Type and extent of injury

Location of injury

266
Q

What cytokines are released from M2 macrophages that have anti-inflammatory effects?

A

IL-10

TGF-β

267
Q

Morphology of a granuloma

A

Epithelioid cells

Giant cells (fused activated macrophages)

Caseous necrosis (central area of necrosis)

268
Q

What stimulates the liver to produce acute phase proteins?

A

IL-1 and IL-6

269
Q

Clinical and pathologic changes associated with the acute-phase response include:

A

Fever

Acute-phase reactants

Leukocytosis

270
Q

How do epithelioid cells present in granulomas form?

A

When activated macrophages develop abundant cytoplasm

271
Q

What acute phase proteins are associated with the acute-phase response?

A

C-reactive protein (CRP)

Fibrinogen

Serum Amyloid A (SAA)

Hepcidin

272
Q

Of the mediators, which is the most important for synthesis and deposition of connective tissue proteins

A

TGF-β

273
Q

What cytokine is produced by TH1 cells and what is it’s function?

A

INF-γ

Activation of M1 macrophages

274
Q

Healing by CT replacement (scarring or fibrosis) typically occurs after substantial tissue destruction through what mechanism?

A

Organization

275
Q

Fibrinous exudates occur commonly in what areas of the body?

A

lining of body cavities, such as the meninges, pericardium and pleura

276
Q

Regeneration of the liver occurs through two mechanisms:

A

Proliferation of remaining hepatocytes

repopulation from progenitor cells

277
Q

What is the triad of sepsis?

A

Disseminated intravascular coagulation

Hypotensive shock

Metabolic disturbances (insulin resistance, hyperglycemia)

278
Q

What tissue types are unable to undergo repair d/t the fact that they cannot proliferate?

A

Brain

Heart

279
Q

Stable cells, parenchyma of solid organs, are considered what kind of tissue?

A

Stable tissues

280
Q

What cells are the source of prostaglandins and leukotrienes?

A

Mast cells

Leukocytes

281
Q

Superoxide anion is converted into hydrogen peroxide (H2O2) through

A

spontaneous dismutation

282
Q

What are acute-phase proteins?

A

Plasma proteins generated in the liver

283
Q

What are the components of a Transudate?

A

low protein

little to no cellular material

low specific gravity

284
Q

Deposition of CT is mediated by what factors?

A

PDGF, FGF-2, TGF-β

285
Q

What types of granules do neutrophils have?

A

small specific granules

large azurophilic granules

286
Q

Functions of the complement system

A

Inflammation

Opsonization

Cell lysis

287
Q

Growth factors involved in tissue repair are released by what cell type?

A

Macrophages activated by tissue injury

288
Q

Ulcerations occur when during healing?

A

When there is inadequate vascularization during healing

289
Q

Contractures occur commonly after repair of injury induced by a burn, what is a contracture?

What are common places for contractures to occur?

A

Excessive contraction by myofibroblasts that leads to deformities in the wound and surrounding tissues

Commonly seen in the palms, soles, and anterior aspect of the thorax

290
Q

Granuloma formation is induced by what cytokine?

A

INF-γ

MOD Exam 1 (5 decks)

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