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COM MOD > Robbins Chapter 3 Key Concepts > Flashcards

Robbins Chapter 3 Key Concepts Flashcards

1
Q

Cells associated with acute respiratory distress syndrome?

A

neutrophils, acute

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2
Q

Cells associated with asthma

A

IgE, eosinophils, acute or chronic

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3
Q

Cells associated with glomerulonephritis

A

antibodies and complement, neutrophils, monocytes, acute

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4
Q

Cells associated with septic shock

A

cytokines, acute

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5
Q

Cells associated with arthritis

A

lymphocytes and macrophages, chronic

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6
Q

Cells associated with atherosclerosis

A

macrophages and lymphocytes, chronic

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7
Q

Cells associated with pulmonary fibrosis

A

macrophages and fibroblasts, chronic

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8
Q

Main components of inflammation

A

vascular reaction and cellular response which are activated by mediators

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9
Q

5Rs of inflammatory response

A

Recognize, Recruit, Remove, Regulate, Repair

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10
Q

5 causes of inflammation

A

infection, trauma, foreign bodies, tissue necrosis, immune response

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11
Q

How do cells recognize microbes or damage

A

specific receptors on macrophages, DCs, and leukocytes, and circulating proteins

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12
Q

Outcomes of acute inflammation

A

elimination of noxious stimulus, decline in reaction, repair of damaged tissues, or persistance can cause chronic inflammation

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13
Q

Vasodilation during acute inflammation

A

induced by histamine causes erythema and stasis

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14
Q

What are the hallmarks of acute inflammation

A

increased vascular permeability, dilation of small blood vessels, accumulation of leukocytes and fluid in tissue

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15
Q

What causes increased vascular permeability during acute inflammation

A

induced by histamine, bradykinin, and leukotrienes to cause gaps in epithelium by retraction of endothelial cells or direct tissue damage (burns) to increase passage of fluid

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16
Q

Lymphatic vessel function in acute inflammation

A

help remove some of the fluid leaked that is causing edema

lymph nodes can become secondarily inflamed via hyperplasia

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17
Q

Leukocyte recruitment process

A

margination, rolling via selectins, integrin activation by chemokines, adhesion via integrins, diapedesis via PECAM

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18
Q

What cytokines promote expression of selectins and integrin ligands on endothelium?

A

TNF and IL-1

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19
Q

What increased the avidity of integrins for their ligands

A

chemokines

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20
Q

What promotes directional migration of leukocytes during leukocyte activation?

A

chemokines

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21
Q

What cell predominates during early inflammation

A

neutrophils which are later replaced by monocytes/macrophages

22
Q

How do leukocytes eliminate microbes and dead cells

A

by phagocytosis followed by destruction in phagolysosome

23
Q

How does destruction occur in the phagolysosome?

A

ROS, iNOS (RNS)

24
Q

Neutrophil Extracellular Traps

A

neutrophils surround the microbe and trap it in fibrils to prevent it from spreading

25
How does tissue injury occur through inflammation
if the phagolysosome releases it's contents into the ECM it can cause damage to cells
26
What are the antiinflammatory cells involved in termination the inflammatory response
IL-10, TGF-b, and inhibiting TNF
27
Function of vasoactive amines in inflammation
vasodilation and increased vascular permeability | ex. histamine
28
What is the general function of arachidonic acid metabolites?
vascular reactions, leukocyte chemotaxis, inflammation | antagonized by lipotoxins
29
Principle cytokines of acute inflammation
TNF and IL-1
30
3 outcomes of complement pathway activation
Inflammation - C3a, C5a Opsonization - C3b MAC complex formation C3bC5b + C6-9
31
Function of kinins
mediate pain, dilation of blood vessels, and increase vascular permeability
32
How does chronic inflammation occur
prolonged host response to persistent stimuli
33
Causes of chronic inflammation
microbes that are resistant to elimination, immune response against self, and toxic substances
34
Characteristics of chronic inflammation
coexisting inflammation, tissue injury, attempted repair by scar tissue, immune response
35
Cellular infiltrate of chronic inflammation
macrophages, lymphocytes, plasma cells, leukocytes
36
Granulomatous inflammation pattern of chronic inflammation
induced by T cells and macrophages in response to microbes resistant to eradication
37
What induces a fever during systemic inflammation
TNF and IL-1 which stimulate prostaglandin production in hypothalamus
38
Acute phase proteins in systemic inflammation
CRP, fibrinogen and SAA which are stimulated by IL-6
39
Leukocytosis in systemic inflammation
cytokines stimulate production of leukocytes from precursors in the bone marrow *more immature neutrophils in blood*
40
Septic Shock triad
decreased blood pressure, widespread intravascular coagulation, and metabolic abnormalities
41
What causes septic shock
overwhelming response of cytokines (TNF and IL-1)
42
Labile tissues
continuously replaced
43
How is cell proliferation controlled during regeneration
by the cell cycle which is stimulated by growth factors and interactions with ECM
44
How is a scar formed for damaged tissue
with connective tissue if the tissue is not capable of proliferation
45
What are the main components of connective tissue repair
angiogenesis, migration and proliferation of fibroblasts, collagen synthesis, and connective tissue remodeling
46
What is the potent cytokine involved in scar formation
TGFb
47
What is ECM deposition dependent on?
MMPs that digest ECM and TIMPs that stop MMPs once no longer needed
48
Main phases of wound healing
inflammation, formation of granulation tissue, and ECM remodeling
49
When does secondary healing occur
extensive scarring and wound contraction
50
2 main conditions that can alter wound healing
infection and diabetes
51
How can keloids be formed
excessive production of ECM
52
How does fibrosis occur
persistent stimulation of collagen synthesis in chronic inflammatory diseases

COM MOD (21 decks)

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