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anaphy lec > Unit 2 Part 3 > Flashcards

Unit 2 Part 3 Flashcards

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
Q

Increased Vascular Permeability events

A
  1. Elevation of the local hydrostatic pressure
  2. Increased permeability of the microvasculature
  3. Leakage of proteinaceous fluid
  4. Stasis
  5. Margination of circulating leukocytes and endothelial activation
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25
Q

general term for swelling

A

edema

26
Q

maintain a “colloid osmotic pressure”

A

Plasma proteins

27
Q

(e.g. heart failure)
and/or colloid pressure (decresased protein synthesis/retention)
pushes out more fluid (transudate) into tissue bed

A

Dysregulation of hydrostatic pressure

28
Q

causes endothelial cells to separate

A

inflammation

29
Q

excess of fluid in the interstitial or serous cavities

A

edema

30
Q

<1.012 gravity
low protein content
ultrafiltrate of blood plasma

A

Transudate

31
Q

> 1.020 gravity high protein concentration,
alteration in the normal permeability of small blood vessels

A

Exudate

32
Q

recruited from the blood
into the extravascular tissue

A

leukocytes

33
Q

predominate in the
inflammatory infiltrate during the first 6 to
24 hours.

A

neutrophils

34
Q

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.

A

neutrophils

35
Q

leukocyte recruitment events

A

margination
rolling
activation
adhesion
transmigration
chemotaxis
phagocytosis
killing

36
Q

leukocyte accumulation at the periphery of vessels.
Fluid leaves the vessel (exudate)
Leukocytes are pushed out of the
central axial column

A

Margination

37
Q

◼ 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

A

Rolling

38
Q

Integrin — by chemokines
Chemotaxis

A

Activation

39
Q

chemotactic cytokines which
support firm adhesion to endothelial cell

A

Chemokines

40
Q

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.

A

Chemotaxis

41
Q

Proteins that function mechanically, by attaching the cell cytoskeleton to the extracellular matrix (ECM), and biochemically, by sensing whether adhesion has occurred

A

Integrins

42
Q

mediated by selectin
family expressed on leukocyte cell
surfaces interacting with their ligands on
endothelial cell

A

Adhesion

43
Q

selectin family

A

◼ E selectin (endothelium)
◼ P selectin (platelets, endothelium)
◼ L selectin (leukocytes)

44
Q

leukocytes migrate through the
vessel wall primarily by squeezing
between cells at intercellular junctions
(diapedesis)

A

Transmigration

45
Q

leukocytes migrate toward sites of infection or injury
locomotion oriented along a chemical gradient

A

Chemotaxis

46
Q

process of coating a particle
Coated microbes are recognized by
receptors on phagocytes

A

Leukocyte Activation
(opsonization)

47
Q

◼ The process of engulfment of solid
particulate material by cells
◼ responsible for eliminating the injurious
agent

A

Phagocytosis

48
Q

3 interrelated steps of phagocytosis

A

Recognition and Attachment
Engulfment
Killing of Degradation

49
Q

◼ Involves the particle
to be ingested by
the leukocyte
◼ Foreign objects
coated with
opsonins IgG and
C3b which attach to
receptors on
polymorph surface

A

Recognition and
Attachment

50
Q
  • Cell membrane fuses around an object
  • this gives rise to ‘regurgitation during feeding’ and enzymatic damage to surrounding tissue
A

Engulfment

51
Q

-H2O2, hypohalous acid (HOC1) produced by myeloperoxidase and superoxides kill bacteria.
-After phagocytosis, neutrophils undergo apoptosis and are ingested by macrophages

A

Killing of Degradation

52
Q

Outcome of Acute Inflammation

A

◼ Complete resolution
◼ Tissue destruction and persistent acute inflammation
◼ Healing by connective tissue replacement
◼ Chronic Inflammation

53
Q

Morphologic patterns of Acute Inflammation (7)

A

Serous
Catarrhal
Fibrinous
Hemorrhagic
Suppurative
Gangrenous
Pseudomembranous

54
Q

◼ Accumulation of excessive clear watery fluid
◼ Blister arising from a burn or viral infection

A

Serous Inflammation

55
Q

◼ Large amounts of fibrinogen pass the vessel wall and fibrins are formed
◼ Fibrinous pericarditis

A

Fibrinous Inflammation

56
Q

◼ Local defect or excavation of the surface of an organ or tissue
◼ Most commonly encountered in the oral mucosa, subcutaneous tissue

A

Ulcerative Inflammation

57
Q

Laboratory Manifestations in Acute Inflammation

A

◼ Leukocytosis
◼ Elevated serum active phase proteins
◼ Increased ESR
◼ Hypercoagulability

58
Q

Inflammation of prolonged duration in which active inflammation, tissue destruction and attempts at repair proceed simultaneously

A

Chronic Inflammation

59
Q

Causes of Chronic
Inflammation

A

-Persistent injury of infection
-Prolonged exposure to potentially toxic
agents
-Autoimmune disease

60
Q

—self-perpetuating
immune reaction that results in tissue
damage and inflammation

A

auto immune disease

61
Q

Morphologic features inflammation

A

Infiltration
Tissue destruction
Healing

62
Q

◼ A special form of chronic inflammation
◼ Characterized by focal activation of
activated macrophages

A

Granulomatous inflammation

63
Q

focal aggregation of
epithelioid macrophages surrounded by
a collar of mononuclear leukocytes

A

Granuloma

anaphy lec (13 decks)

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