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22 spring: immunology > Test 2: lecture 3 and 4 wound healing > Flashcards

Test 2: lecture 3 and 4 wound healing Flashcards

1
Q

three main type of inflammation

A

actue

granulomatous

chronic

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2
Q

___ has a short duration, edema and involves mainly neutrophils

A

acute inflammation

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3
Q

___ has a distinctive pattern of chronic inflammation, activated macrophages, +/- multi-nucleated giant cells

A

granulomatous inflammation

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4
Q

___ occurs over a long duration, involves mainly lymphocytes and macrophages, is fibrosis and creates new blood vessels

A

chronic inflammation

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5
Q

difference between acute and chronic inflammation

A

chronic produces fibrosis and new blood vessels (angiogenesis)

acute → mainly neutrophils

chronic → lymphocyte and macrophages

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6
Q

Acute inflammation is cause by ___in blood flow (redness & warmth)

A

Increase

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7
Q

acute inflammation causes edema results from ___hydrostatic pressure (vasodilation) and ____intravascular osmotic pressure (protein leakage)

A

increased

lowered

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8
Q

acute inflammation - ___ emigrate from microcirculation and accumulate in the focus of injury

A

Leukocytes(white blood cells specifically neutrophils)

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9
Q

Plasma proteins in blood maintain a “___pressure” to help draw fluid that leaks out into tissue bed via hydrostatic pressure

A

colloid osmotic

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10
Q

how does edema happen

A

tight junctions between endothelial cells in the vessels become loose and let fluid from the vessels to leak out into the extracellular space

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11
Q

movement of cell across endothelium

A

extravasation or diapedesis

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12
Q

steps of extravasation

A

In the lumen: margination, rolling, and adhesion
– Migration across the endothelium (diapedesis)
– Migration in the interstitial tissue (chemotaxis)

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13
Q

sequence of leukocyte emigration

A

Neutrophils predominate during the first 6 to 24 hours

Monocytes in 24 to 48 hours

Induction/activation of different adhesion molecule pairs and specific chemotactic factors in different phases of inflammation

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14
Q

this graph is for what type of inflammation?

A

acute

edema → neutrophils → monocytes

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15
Q

label

A
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16
Q

if acute inflammation does not resolve what can happen

A

Abscess formation

Fibrosis
– After substantial tissue destruction
– In tissues that do not regenerate
– After abundant fibrin exudation, especially in serous cavities (pleura, peritoneum)

Progression to chronic inflammation

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17
Q

____: Outpouring of thin fluid (___effusion, blisters)

A

serous inflammation

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18
Q

____: Body cavities; leakage of fibrin; may lead to scar tissue (adhesions)

A

Fibrinous inflammation

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19
Q

____: Pus or purulent exudate (neutrophils, debris, edema fluid); abscess: localized collections of pus

A

Suppurative (purulent) inflammation

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20
Q

___: Local defect of the surface of an organ or tissue produced by the sloughing (shedding) of inflammatory necrotic tissue

A

Ulcers

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21
Q

systemic manifestations of acute inflammation

A

Autonomic
– Redirection of blood flow from skin to deep vascular beds minimizes heat loss – Increased pulse and blood pressure

Behavioral
– Shivering (rigors), chills (search for warmth), anorexia (loss of appetite), somnolence(drowsy), and malaise

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22
Q

autonomic systemic manifestations of acute inflammation

A

Autonomic
– Redirection of blood flow from skin to deep vascular beds minimizes heat loss – Increased pulse and blood pressure

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23
Q

behavioral systemic manifestations of acute inflammation

A

Behavioral
– Shivering (rigors), chills (search for warmth), anorexia (loss of appetite), somnolence, and malaise

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24
Q

Leukocytosis

A

increased leukocyte count in the blood

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25
Q

___ will increase due to bacterial infections

A

Neutrophilia

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26
Q

___ increases in the blood due to infectious mononucleosis, mumps,
measles

A

lymphocytosis

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27
Q

___ increases in the blood due to parasites, asthma and hay fever

A

eosinophilia

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28
Q

___ results from Typhoid fever, some viruses, rickettsiae, protozoa

A

Leukopenia: reduced leukocyte count

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29
Q

chronic inflammation can caused by ___

A

May follow acute inflammation or begin asymptomatically through unknown means (autoimmunity)

Persistent infections
– Treponema pallidum [syphilis], viruses, fungi, parasites

Exposure to toxic agents
– Exogenous: silica (silicosis)
– Endogenous: Uric acid crystals (Gout), toxic plasma lipid components (atherosclerosis)

Autoimmunity
– Rheumatoid arthritis, systemic lupus erythematosus

Active inflammation, tissue destruction, and attempts at repair are proceeding simultaneously

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30
Q

Chronic Inflammation is characterized by infiltration with ____ cells. Tissue ___ caused by the inflammatory cells). Healing by replacement of damaged tissue by ___

A

mononuclear (macrophages, lymphocytes, and plasma cells)

destruction

connective tissue (fibrosis) and new blood vessels (angiogenesis)

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31
Q

what kinds of cells invade for chronic vs acute inflammation

A

chronic= mononuclear cells

acute= polynucleated cell (neutrophil, monocytes/macrophages, lymphocytes/plasma cells)

(macrophages, lymphocytes, and plasma cells)

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32
Q

activated macrophages can cause tissue injury by ___

A

toxic oxygen metabolites

proteases

neutrophil chemotactic factors

coagulation factor

AA metabolites

Nitric oxide

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33
Q

activated macrophages can cause fibrosis by ___

A

growth factors (PDGF, FGF, TGFbeta)

Fibrogenic cytokines

angiogenesis factor (FGF)

“remodeling” collagenesis

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34
Q

Monocytes begin to emigrate into tissues early in inflammation where
they transform into ____

A

the larger phagocytic cell known as the macrophage

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35
Q

during chronic inflammation, activated of ___ results in secretion of biologically active products

A

macrophages

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36
Q

Lymphocytes and macrophages interact in a ____ fashion

A

bi-directional

(can calm each other down or hype each other up)

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37
Q

eosinophils in chronic inflammation is a reaction to ___ and indicates ___

A

immune reaction mediated by IgE

parasitic infection- eosinophil granules contain a protein that is toxic to parasites

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38
Q

___ cells release mediators (histamine) and cytokines

A

mast cells

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39
Q

Granulomatous Inflammation is a distinctive pattern of ___inflammation. Predominant cell type is ___ with a modified epithelial-like (epithelioid) appearance. ___ may or may not be present

A

chronic

activated macrophage- look weird (wraps around infection)

Giant cells

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40
Q

granulomas can form ___

A

around a foreign body (suture)

or caused by an insoluble or poorly soluble particles elicit
a cell-mediated immune response (parasite egg)

41
Q

some preformed mediators in secretory granules are ___

A

histamine made by mast cells, basophils

serotonin made by platelets

lysosomal enzymes made by neutrophils and macrophages

42
Q

why does histamine work so quickly

A

preformed mediator that is sitting in secretory granules inside mast cells

waiting to be released

43
Q

what are some newly synthesized mediators

A

prostaglandins made by leukocytes

leukotrienes made by leukocytes

platelet activating factors made by leukocytes

activated oxygen species made by leukocytes

nitric oxide made by macrophages

cytokines made by lymphocytes, macrophages, EC

44
Q

two major types of mediators

A

preformed in secretory granules

newly synthesized

45
Q

what chemical mediators have vasoactive properties

A
46
Q

what chemical mediators have chemotactic properties

A
47
Q

histamine made by ___ .

A

Mast cells (also basophils and platelets

48
Q

how is histamine released

A

IgE binds to Fc on Mast cell

antigen (allergen) binds to the IgE on mast cells

releases histamine- containing granules

49
Q

histamine ___ arterioles and ___ permeability of venules (wheal and flare reaction)

A

dilates

increases

50
Q

complement are proteins found in greatest concentration in
the ___

A

plasma

51
Q

complement requires activation and causes ___ vascular permeability and ___

A

Increased

vasodilation

52
Q

complement Increase ___adhesion, chemotaxis, and activation

A

leukocyte

53
Q

____ are small peptide released from plasma precursors

A

bradykinin

54
Q

bradykinin ___ vascular permeability and ___ blood vessels

A

increase

dilates

55
Q

____ cause pain and have a rapid inactivation

A

bradykinin

56
Q

Platelet Activating Factor is a subclass of ___. Synthesized by stimulated platelets, leukocytes and endothelium.

A

phospholipids

57
Q

___ cause platelet aggregation, vaso___ and broncho____

A

platelet activating factor

Vasoconstriction and bronchoconstriction

58
Q

cytokines are proteins produced by many cell types (principally released by activated lymphocytes & macrophages) and will ___ the function of other cell types

A

modulate (increase or decrease)

59
Q

____ and tumor necrosis factor (TNF) are the major cytokines that mediate
inflammation

A

Interleukin-1 (IL-1) (acute inflammation)

60
Q

___ are small proteins that act primarily as chemoattractants for specific types of leukocytes

A

chemokines

61
Q

chemokines stimulate ___recruitment in inflammation

A

leukocyte

62
Q

chemokines control the normal ___through
tissues

A

migration of cells

(organogenesis and maintenance of tissue organization)

63
Q

___ are cationic proteins increase vascular permeability,
immobilize neutrophils, chemotactic for mononuclear phagocytes

A

neutrophil granules

64
Q

___ are produced during phagocytosis by neutrophils

(“respiratory burst”)

A

oxygen-derived free radicals

65
Q

oxygen-derived free radicals cause ___ including endothelium

A

tissue damage

66
Q

mediators that cause chemotaxis and leukocyte activation

A

– Complement (C5a)
– Leukotriene B
– Chemokines
– IL-1, TNF
– Bacterial products

67
Q

mediators that cause fever

A

Interleukin-1
– Tumor necrosis factor
– Prostaglandins

68
Q

mediators that cause pain

A

prostaglandins

bradykinin

69
Q

___ mediators cause tissue damage

A

Neutrophil and macrophage lysosomal enzymes
– Oxygen metabolites
– Nitric oxide

70
Q

Interleukin-1 (IL-1) and TNF are released during

A

(acute inflammation)

cytokines made by many cell types ( principally released by activated lymphocytes and macrophages)

71
Q

three phases of wound healing

A

Inflammatory Phase

Proliferative Phase

Remodeling Phase

72
Q

steps of wound healing

  1. Injury induces ___inflammation
  2. ___ cells regenerate
  3. Both parenchymal and ___ cells migrate and
    proliferate
  4. ___ is produced
  5. Parenchyma and connective tissue matrix ___
  6. Increase in wound strength due to ___deposition
A

acute

Parenchymal

connective tissue

Extracellular matrix

remodel

collagen

73
Q

granulation tissue

A

Hallmark of healing

  • Term comes from soft, pink, granular appearance when viewed from the surface of a wound
  • Histology: Proliferation of small blood vessels and fibroblasts; tissue often edematous
74
Q

when does proliferative phase of wound healing occur?

A

when wound is covered with epithelium and lasts 7days to 6 week

75
Q

___ production is hallmark of the proliferative phase of wound healing

A

collagen

76
Q

during the inflammatory phase there is ___ for 4-6 days where exposed ___ activates clotting cascade. ___ acts as scaffolding and concentrate cytokines and growth factors

A

hemostasis and inflammation

collagen

fibrin clot

77
Q

___ are recruited in the 1st 48 hours of the inflammatory stage of wound healing

A

granulocytes

attracted by inflammatory mediators

78
Q

during the inflammatory phase of wound healing monocytes are attracted to an area by complement are activated by ___

A

fibrin and foreign body material

reach a max after 24 hrs, remain for week

79
Q

macrophages are essential for progression into the ___ phase of wound healing

A

proliferative

three stages: inflammatory, proliferative, remodeling

80
Q

activated macrophages mediates

A

angiogenesis, fibroplasia and make nitric oxide, they also secrete collagenases

81
Q

3 key features of the proliferative phase of the wound healing process

A

Epithelization, Angiogenesis and Provisional Matrix Formation

(begins when wound is covered by epithelium, day 4-14, production of collagen)

82
Q

___ are a major source of the collagen in the proliferative phase of wound healing

A

fibroblasts

83
Q

epithelialization

A

cells next to a break will spread to cover area and then grow and divide

Basal epithelial cells at the wound margin flatten (mobilize) and migrate into the open wound

Basal cells at margin multiply (mitosis) in horizontal direction

Basal cells behind margin undergo vertical growth (differentiation)

84
Q

mitosis vs differentiation

A

Basal cells at margin multiply (mitosis) in horizontal direction

Basal cells behind margin undergo vertical growth (differentiation)

85
Q

____ are the work horse of wound repair

A

fibroblast

86
Q

fibroblasts produce granulation tissues through ___ signals

A

PDGF and EGF

87
Q

Fibroblasts produce ___

A

Collagen type III
– Glycosaminoglycans
– Fibronectin
– Elastin fibers

88
Q

Tissue fibroblasts become myofibroblasts induced by ____

A

TGF-b1

89
Q

___ are in charge of moving skin during wound contraction

A

myofibroblasts - contractile properties

90
Q

steps of collagen homeostasis

A

Days 3 - 7 week
• Collagen production begins

Days 7 – 42
• Synthesis with a net GAIN of collagen
• Initial increase in tensile strength due to increase amount of collagen

Days 42+
• Remodeling with No net collagen gain

91
Q

during maturation phase ___ is replaced by ___

A

type III collagen

Type 1 collagen

92
Q

during the maturation phase of wound healing the wound will increase in strength by ___

A

Collagen organization

Cross linking of collagen

93
Q

collagen synthesis can not take place during ___

A

hypoxia, fibroblasts are oxygen sensitive

healing is energy dependent- proliferative phase has increased metabolism and protein synthesis

94
Q

radiation therapy causes ___

A

fibroblast defects are the central problem in thehealing of chronic radiation injury

95
Q

what medication can decrease wound healing

A

steroids - interferes with fibrogenesis, angiogenesis, and
wound contraction

vitamin A deficiency

Vitamin C deficiency - Vit C is needed to make collagen

too much Vitamin E :

96
Q

what will glutamine do to wound healing?

A

Enhance actions of lymphocytes, macrophages and neutrophils

97
Q

what will glycine do to wound healing?

A

Inhibitory effect on leukocytes, might reduce inflammation related tissue injury

98
Q

what will zinc do to wound healing

A

common constituent of dozens of enzymes

  • Influences B and T cell activity
  • epithelial and fibroblastic proliferation is impaired in patients with low serum zinc levels
99
Q

regeneration vs healing

A

regeneration → duplicate original

wound healing→ add something new (scar → patching up)

chronic inflammation → (granuloma induced inflammation)→ too much collagen → fibrous deposition

22 spring: immunology (23 decks)

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