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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
Q

How does tissue injury occur through inflammation

A

if the phagolysosome releases it’s contents into the ECM it can cause damage to cells

26
Q

What are the antiinflammatory cells involved in termination the inflammatory response

A

IL-10, TGF-b, and inhibiting TNF

27
Q

Function of vasoactive amines in inflammation

A

vasodilation and increased vascular permeability

ex. histamine

28
Q

What is the general function of arachidonic acid metabolites?

A

vascular reactions, leukocyte chemotaxis, inflammation

antagonized by lipotoxins

29
Q

Principle cytokines of acute inflammation

A

TNF and IL-1

30
Q

3 outcomes of complement pathway activation

A

Inflammation - C3a, C5a
Opsonization - C3b
MAC complex formation C3bC5b + C6-9

31
Q

Function of kinins

A

mediate pain, dilation of blood vessels, and increase vascular permeability

32
Q

How does chronic inflammation occur

A

prolonged host response to persistent stimuli

33
Q

Causes of chronic inflammation

A

microbes that are resistant to elimination, immune response against self, and toxic substances

34
Q

Characteristics of chronic inflammation

A

coexisting inflammation, tissue injury, attempted repair by scar tissue, immune response

35
Q

Cellular infiltrate of chronic inflammation

A

macrophages, lymphocytes, plasma cells, leukocytes

36
Q

Granulomatous inflammation pattern of chronic inflammation

A

induced by T cells and macrophages in response to microbes resistant to eradication

37
Q

What induces a fever during systemic inflammation

A

TNF and IL-1 which stimulate prostaglandin production in hypothalamus

38
Q

Acute phase proteins in systemic inflammation

A

CRP, fibrinogen and SAA which are stimulated by IL-6

39
Q

Leukocytosis in systemic inflammation

A

cytokines stimulate production of leukocytes from precursors in the bone marrow
more immature neutrophils in blood

40
Q

Septic Shock triad

A

decreased blood pressure, widespread intravascular coagulation, and metabolic abnormalities

41
Q

What causes septic shock

A

overwhelming response of cytokines (TNF and IL-1)

42
Q

Labile tissues

A

continuously replaced

43
Q

How is cell proliferation controlled during regeneration

A

by the cell cycle which is stimulated by growth factors and interactions with ECM

44
Q

How is a scar formed for damaged tissue

A

with connective tissue if the tissue is not capable of proliferation

45
Q

What are the main components of connective tissue repair

A

angiogenesis, migration and proliferation of fibroblasts, collagen synthesis, and connective tissue remodeling

46
Q

What is the potent cytokine involved in scar formation

A

TGFb

47
Q

What is ECM deposition dependent on?

A

MMPs that digest ECM and TIMPs that stop MMPs once no longer needed

48
Q

Main phases of wound healing

A

inflammation, formation of granulation tissue, and ECM remodeling

49
Q

When does secondary healing occur

A

extensive scarring and wound contraction

50
Q

2 main conditions that can alter wound healing

A

infection and diabetes

51
Q

How can keloids be formed

A

excessive production of ECM

52
Q

How does fibrosis occur

A

persistent stimulation of collagen synthesis in chronic inflammatory diseases

COM MOD (21 decks)

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