Inflammation and Repair Flashcards

1
Q

Steps in LEUKOCYTE RECRUITMENT

A

MRATC
1. Margination
2.Rolling
3.Adhesion
4.Transmigration
5. Chemotaxis

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2
Q

The process of leukocyte ACCUMULATION at the PERIPHERY of the blood. vessels

A

Margination

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3
Q

TRANSIENT BINDING and DETACHMENT of leukocytes to the endothelium
Mediated by SELECTINS

A

Rolling

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4
Q

FRIM ADHESION of leukocytes to the endothelium
Mediated by INTEGRIN

A

Adhesion

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5
Q

The process of MIGRATION of leukocytes through the endothelium
Mediated by PECAM-1/CD31

A

Transmigration or Diapedesis

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6
Q

Process of leukocyte migration toward sites of infection or injury along a chemical gradient mediated by exogenous or endogenous substances

A

Chemotaxis

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7
Q

Type of inflammatory mediators that are normally SEQUESTERED in INTRACELLULAR GRANULES
Can be rapidly secreted by granule exocytosis or are synthesized de novo in response to a stimulus

A

CELL DERIVED MEDIATORS

histamine
serotonin
cytokines
arachidonic acid derivatives (prostaglandins and//leukotrienes)

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8
Q

Type of inflammatory mediators that are PRODUCED MAINLY in the LIVER
Present in the circulation as INACTIVE precursors that must be activated by PROTEOLYTIC cleavage to acquire their biologic properties

A

PLASMA DERIVED MEDIATORS

complement
coagulation system
kinin system

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9
Q

Vasoactive amine found in PLATELETS and NEUROENDOCRINE CELLS
Causes VASOCONSTRICTION

A

Serotonin

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10
Q

VASODILATION

A

PGI2 (Prostacyclin)
PGE1 (Prostaglandin)
PGE2 (Dinoprostone)
PGD2

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11
Q

VASOCONSTRICTION

A

TXA2
LTC4
LTD4
LTE4

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12
Q

INCREASED VASCULAR PERMEABILITY

A

LTC4
LTD4
LTE4

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13
Q

CHEMOTAXIS, LEUKOCYTE ADHESION

A

LTB4
Hydroxyeicosatetratenoic acid (HETE)

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14
Q

Most abundant complement

A

C3

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15
Q

Complement that acts as OPSONIN

A

C3b

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16
Q

ANAPHYLATOXINS

A

C3a, C4a, C5a

17
Q

MEMBRANE ATTACK COMPLEX (MAC)

18
Q

Deficiency of the ff complement-related protein causes HEREDITARY ANGIOEDEMA

A

C1 inhibitor deficiency

19
Q

Deficiency of the ff complement protein increases susceptibility to INFECTIONS involving PYOGENIC BACTERIA

20
Q

Deficiency of the ff complement proteins increases susceptibility to IMMUNE COMPLEX MEDIATED DISEASE

A

C1q, C2 and C4

21
Q

Deficiency of the ff complement protein increases susceptibility to NEISSERIA INFECTIONS

22
Q

Main cells involved in CHRONIC INFLAMMATION

A

monocytes/macrophages
lymphocytes

23
Q

Collections of ACTIVATED MACROPHAGES, some of which form MULTINUCLEATED GIANT CELLS often w/ T lymphocytes and sometimes associated w/ CENTRAL NECROSIS

24
Q

2 kinds of cells seen in GRANULOMAS

A

Epithelioid cells
Giant cells

25
Precursor cell of epithelioid cells and giant cells
Macrophages
26
Type of tissue whose cells can READILY REGENERATE as long as the pool of stem cell is preserved
LABILE TISSUES bone marrow vaginal epithelium
27
Type of tissue whose cells are considered to be terminally differentiated and are NON-PROLIFERATIVE in POSTNATAL LIFE
PERMANENT TISSUES neurons cardiac muscle
28
Type of tissue whose cells are quiescent and have only minimal replicative activity in their normal state Capable of PROLIFERATING IN RESPONSE TO INJURY OR LOSS OF TISSUE MASS
STABLE TISSUES smooth muscles endothelium liver parenchyma
29
Type of repair that happens in LABILE and STABLE tissues Influenced by GROWTH FACTORS
Regeneration
30
Type of repair that happens in CHRONIC, SEVERE INFLAMMATION and PERMANENT TISSUES
Connective Tissue Deposition
31
Steps in healing by CT deposition
1. Angiogenesis 2. Formation of granulation tissue 3. Remodeling of the scar
32
Most notable growth factor in ANGIOGENESIS
VEGF
33
Most important CYTOKINE for synthesis and deposition of CT
TGF-B
34
Hallmark of REPAIR
Granulation tissue
35
Components of GRANULATION TISSUE
1. Proliferation of FIBROBLASTS 2. LOOSE CT 3. Angiogenesis 4. Inflammatory cells
36
Most important source of growth factors during repair
Macrophage
37
Factors that impede repair
infections DM vitamin C deficiency glucocorticoids (-) TGF-B pressure poor perfusion foreign bodies location of injury