Unit 2 Part 3 Flashcards

(64 cards)

1
Q

COMPLEX response to injurious
agents

A

inflammation

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1
Q

COMPLEX response to injurious
agents

A

inflammation

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2
Q

leads as to the healing and reconstitution of the damaged tissue
(repair)

A

inflammation

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3
Q

Aims of inflammation

A
  • Eliminate the initial cause of cell injury
  • Remove necrotic cells and tissue
  • Initiate the process of repair
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4
Q

INFLAMMATION is part of a broader
protective response OR

A

innate immunity

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5
Q

Components of the inflammatory
process

A

white blood cells and
plasma proteins

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6
Q

Inflammation is terminated when

A

offending agent is eliminated
secreted mediators are broken down

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7
Q

inflammation is potentially harmful process if

A

Components are capable of destroying microbes
-injure

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8
Q

no foreign substances to fight leads to

A

autoimmunity

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9
Q

inflammatory process is tightly regulated by

A

immune system

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10
Q

causes of inflammation

A

bacteria
viral
protozoal
fungal
immunological
chemical, toxins
tumor
radiation

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11
Q

5 ancient cardinal signs of inflammatory

A

tumor-swelling
rubor-redness
calor-warmth
dolor-pain
functio laesa-loss of function

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12
Q

systemic manifestations of inflammation

A

fever
chills
myalgia
discomfort

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13
Q

Increased blood flow due to vascular dilatation gives

A

redness and heat
rubor and calor

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14
Q

Increased vascular permeability gives edema causing

A

tissue swelling
tumor

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15
Q

Certain chemical mediators stimulate sensory nerve
endings giving

A

pain
dolor

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16
Q

Pain and swelling result in loss of

A

function
functio laesa

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17
Q

features of acute inflammation

A

fast mins or hrs, neutrophil infiltrate, mild and self-limited, prominent

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18
Q

features of chronic inflammation

A

slow days, monocytes infiltrate, severe and progressive, less prominent and subtle

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19
Q

rapid response to an injurious agent
deliver mediators of host defense-leukocytes and plasma proteins

A

acute inflammation

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20
Q

stimuli for acute inflamation

A

infection
necrosis
foreign bodies
immune reactions

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21
Q

Events of Acute Inflammation

A

VASCULAR:
hemodynamic/ Vasoactive changes
increased vascular permeability
CELLULAR
leukocyte recruitment

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22
Q

changes in vascular flow and caliber
earliest manifestation

A

hemodynamic/vasoactive changes

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23
Q

hemodynamic events

A
  1. vasoconstrict
  2. vasodilation
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24
Increased Vascular Permeability events
3. Elevation of the local hydrostatic pressure 4. Increased permeability of the microvasculature 5. Leakage of proteinaceous fluid 6. Stasis 7. Margination of circulating leukocytes and endothelial activation
25
general term for swelling
edema
26
maintain a “colloid osmotic pressure”
Plasma proteins
27
(e.g. heart failure) and/or colloid pressure (decresased protein synthesis/retention) pushes out more fluid (transudate) into tissue bed
Dysregulation of hydrostatic pressure
28
causes endothelial cells to separate
inflammation
29
excess of fluid in the interstitial or serous cavities
edema
30
<1.012 gravity low protein content ultrafiltrate of blood plasma
Transudate
31
>1.020 gravity high protein concentration, alteration in the normal permeability of small blood vessels
Exudate
32
recruited from the blood into the extravascular tissue
leukocytes
33
predominate in the inflammatory infiltrate during the first 6 to 24 hours.
neutrophils
34
more numerous in the blood respond more rapidly to chemokines may attach more firmly to the adhesion molecules short-lived, they die by apoptosis and disappear within 24 to 48 hours.
neutrophils
35
leukocyte recruitment events
margination rolling activation adhesion transmigration chemotaxis phagocytosis killing
36
leukocyte accumulation at the periphery of vessels. Fluid leaves the vessel (exudate) Leukocytes are pushed out of the central axial column
Margination
37
◼ Leukocytes tumble on the endothelial surface, transiently sticking along the way. ◼ This weak and transient adhesion ◼ Enables leukocytes to slow down and travel along the endothelial surface
Rolling
38
Integrin --- by chemokines Chemotaxis
Activation
39
chemotactic cytokines which support firm adhesion to endothelial cell
Chemokines
40
movement of a motile cell or organism, or part of one, in a direction corresponding to a gradient of increasing or decreasing concentration of a particular substance.
Chemotaxis
41
Proteins that function mechanically, by attaching the cell cytoskeleton to the extracellular matrix (ECM), and biochemically, by sensing whether adhesion has occurred
Integrins
42
mediated by selectin family expressed on leukocyte cell surfaces interacting with their ligands on endothelial cell
Adhesion
43
selectin family
◼ E selectin (endothelium) ◼ P selectin (platelets, endothelium) ◼ L selectin (leukocytes)
44
leukocytes migrate through the vessel wall primarily by squeezing between cells at intercellular junctions (diapedesis)
Transmigration
45
leukocytes migrate toward sites of infection or injury locomotion oriented along a chemical gradient
Chemotaxis
46
process of coating a particle Coated microbes are recognized by receptors on phagocytes
Leukocyte Activation (opsonization)
47
◼ The process of engulfment of solid particulate material by cells ◼ responsible for eliminating the injurious agent
Phagocytosis
48
3 interrelated steps of phagocytosis
Recognition and Attachment Engulfment Killing of Degradation
49
◼ Involves the particle to be ingested by the leukocyte ◼ Foreign objects coated with opsonins IgG and C3b which attach to receptors on polymorph surface
Recognition and Attachment
50
- Cell membrane fuses around an object - this gives rise to 'regurgitation during feeding' and enzymatic damage to surrounding tissue
Engulfment
51
-H2O2, hypohalous acid (HOC1) produced by myeloperoxidase and superoxides kill bacteria. -After phagocytosis, neutrophils undergo apoptosis and are ingested by macrophages
Killing of Degradation
52
Outcome of Acute Inflammation
◼ Complete resolution ◼ Tissue destruction and persistent acute inflammation ◼ Healing by connective tissue replacement ◼ Chronic Inflammation
53
Morphologic patterns of Acute Inflammation (7)
Serous Catarrhal Fibrinous Hemorrhagic Suppurative Gangrenous Pseudomembranous
54
◼ Accumulation of excessive clear watery fluid ◼ Blister arising from a burn or viral infection
Serous Inflammation
55
◼ Large amounts of fibrinogen pass the vessel wall and fibrins are formed ◼ Fibrinous pericarditis
Fibrinous Inflammation
56
◼ Local defect or excavation of the surface of an organ or tissue ◼ Most commonly encountered in the oral mucosa, subcutaneous tissue
Ulcerative Inflammation
57
Laboratory Manifestations in Acute Inflammation
◼ Leukocytosis ◼ Elevated serum active phase proteins ◼ Increased ESR ◼ Hypercoagulability
58
Inflammation of prolonged duration in which active inflammation, tissue destruction and attempts at repair proceed simultaneously
Chronic Inflammation
59
Causes of Chronic Inflammation
-Persistent injury of infection -Prolonged exposure to potentially toxic agents -Autoimmune disease
60
—self-perpetuating immune reaction that results in tissue damage and inflammation
auto immune disease
61
Morphologic features inflammation
Infiltration Tissue destruction Healing
62
◼ A special form of chronic inflammation ◼ Characterized by focal activation of activated macrophages
Granulomatous inflammation
63
focal aggregation of epithelioid macrophages surrounded by a collar of mononuclear leukocytes
Granuloma