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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
\_\_\_ will increase due to bacterial infections
Neutrophilia
26
\_\_\_ increases in the blood due to infectious mononucleosis, mumps, measles
lymphocytosis
27
\_\_\_ increases in the blood due to parasites, asthma and hay fever
eosinophilia
28
\_\_\_ results from Typhoid fever, some viruses, rickettsiae, protozoa
Leukopenia: **reduced** leukocyte count
29
chronic inflammation can caused by \_\_\_
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
30
Chronic Inflammation is characterized by infiltration with ____ cells. Tissue ___ caused by the inflammatory cells). Healing by replacement of damaged tissue by \_\_\_
**mononuclear** (macrophages, lymphocytes, and plasma cells) **destruction** connective tissue **(fibrosis)** and new blood vessels **(angiogenesis)**
31
what kinds of cells invade for chronic vs acute inflammation
**chronic= mononuclear cells** **acute= polynucleated** cell (neutrophil, monocytes/macrophages, lymphocytes/plasma cells) | (macrophages, lymphocytes, and plasma cells)
32
activated macrophages can cause tissue injury by \_\_\_
toxic oxygen metabolites proteases neutrophil chemotactic factors coagulation factor AA metabolites Nitric oxide
33
activated macrophages can cause fibrosis by \_\_\_
growth factors (PDGF, FGF, TGFbeta) Fibrogenic cytokines angiogenesis factor (FGF) “remodeling” collagenesis
34
Monocytes begin to emigrate into tissues early in inflammation where they transform into \_\_\_\_
the larger phagocytic cell known as the **macrophage**
35
during chronic inflammation, activated of ___ results in secretion of biologically active products
macrophages
36
Lymphocytes and macrophages interact in a ____ fashion
bi-directional (can calm each other down or hype each other up)
37
eosinophils in chronic inflammation is a reaction to ___ and indicates \_\_\_
immune reaction mediated by **IgE** **parasitic infection-** eosinophil granules contain a protein that is toxic to parasites
38
\_\_\_ cells release mediators (histamine) and cytokines
mast cells
39
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
chronic activated macrophage- look weird (wraps around infection) Giant cells
40
granulomas can form \_\_\_
around a foreign body (suture) or caused by an insoluble or poorly soluble particles elicit a cell-mediated immune response (parasite egg)
41
some preformed mediators in secretory granules are \_\_\_
**histamine** made by mast cells, basophils **serotonin** made by platelets **lysosomal** enzymes made by neutrophils and macrophages
42
why does histamine work so quickly
**preformed mediator** that is sitting in secretory granules inside mast cells waiting to be released
43
what are some newly synthesized mediators
**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
two major types of mediators
preformed in secretory granules newly synthesized
45
what chemical mediators have vasoactive properties
46
what chemical mediators have chemotactic properties
47
histamine made by ___ .
Mast cells (also basophils and platelets
48
how is histamine released
IgE binds to Fc on Mast cell antigen (allergen) binds to the **IgE** on mast cells releases histamine- containing granules
49
histamine ___ arterioles and ___ permeability of venules (wheal and flare reaction)
dilates increases
50
complement are proteins found in greatest concentration in the \_\_\_
plasma
51
complement requires activation and causes ___ vascular permeability and \_\_\_
Increased vasodilation
52
complement Increase \_\_\_adhesion, chemotaxis, and activation
leukocyte
53
\_\_\_\_ are small peptide released from plasma precursors
bradykinin
54
bradykinin ___ vascular permeability and ___ blood vessels
increase dilates
55
\_\_\_\_ cause pain and have a rapid inactivation
bradykinin
56
Platelet Activating Factor is a subclass of \_\_\_. Synthesized by stimulated platelets, leukocytes and endothelium.
phospholipids
57
\_\_\_ cause platelet aggregation, vaso\_\_\_ and broncho\_\_\_\_
platelet activating factor Vasoconstriction and bronchoconstriction
58
cytokines are proteins produced by many cell types (principally released by activated lymphocytes & macrophages) and will ___ the function of other cell types
modulate (increase or decrease)
59
\_\_\_\_ and tumor necrosis factor (TNF) are the major cytokines that mediate inflammation
Interleukin-1 (IL-1) (acute inflammation)
60
\_\_\_ are small proteins that act primarily as chemoattractants for specific types of leukocytes
chemokines
61
chemokines stimulate \_\_\_recruitment in inflammation
leukocyte
62
chemokines control the normal \_\_\_through tissues
migration of cells (organogenesis and maintenance of tissue organization)
63
\_\_\_ are cationic proteins increase vascular permeability, immobilize neutrophils, chemotactic for mononuclear phagocytes
neutrophil granules
64
\_\_\_ are produced during phagocytosis by neutrophils | (“respiratory burst”)
oxygen-derived free radicals
65
oxygen-derived free radicals cause ___ including endothelium
tissue damage
66
mediators that cause chemotaxis and leukocyte activation
– Complement (C5a) – Leukotriene B – Chemokines – IL-1, TNF – Bacterial products
67
mediators that cause fever
Interleukin-1 – Tumor necrosis factor – Prostaglandins
68
mediators that cause pain
prostaglandins bradykinin
69
\_\_\_ mediators cause tissue damage
Neutrophil and macrophage lysosomal enzymes – Oxygen metabolites – Nitric oxide
70
Interleukin-1 (IL-1) and TNF are released during
(acute inflammation) cytokines made by many cell types ( principally released by activated lymphocytes and macrophages)
71
three phases of wound healing
Inflammatory Phase Proliferative Phase Remodeling Phase
72
steps of wound healing ## Footnote 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
acute Parenchymal connective tissue Extracellular matrix remodel collagen
73
granulation tissue
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
when does proliferative phase of wound healing occur?
when wound is covered with epithelium and lasts 7days to 6 week
75
\_\_\_ production is hallmark of the proliferative phase of wound healing
collagen
76
during the inflammatory phase there is ___ for 4-6 days where exposed ___ activates clotting cascade. ___ acts as scaffolding and concentrate cytokines and growth factors
hemostasis and inflammation collagen fibrin clot
77
\_\_\_ are recruited in the 1st 48 hours of the inflammatory stage of wound healing
granulocytes attracted by inflammatory mediators
78
during the inflammatory phase of wound healing monocytes are attracted to an area by complement are activated by \_\_\_
fibrin and foreign body material reach a max after 24 hrs, remain for week
79
macrophages are essential for progression into the ___ phase of wound healing
proliferative three stages: inflammatory, proliferative, remodeling
80
activated macrophages mediates
angiogenesis, fibroplasia and make nitric oxide, they also secrete collagenases
81
3 key features of the proliferative phase of the wound healing process
Epithelization, Angiogenesis and Provisional Matrix Formation (begins when wound is covered by epithelium, day 4-14, production of collagen)
82
\_\_\_ are a major source of the collagen in the proliferative phase of wound healing
fibroblasts
83
epithelialization
**cells next to a break will spread to cover area and then grow and divide** ## Footnote 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
mitosis vs differentiation
Basal cells at margin multiply **(mitosis)** in horizontal direction Basal cells behind margin undergo vertical growth **(differentiation)**
85
\_\_\_\_ are the work horse of wound repair
fibroblast
86
fibroblasts produce granulation tissues through ___ signals
PDGF and EGF
87
Fibroblasts produce \_\_\_
Collagen type III – Glycosaminoglycans – Fibronectin – Elastin fibers
88
Tissue fibroblasts become myofibroblasts induced by \_\_\_\_
TGF-b1
89
\_\_\_ are in charge of moving skin during wound contraction
myofibroblasts - contractile properties
90
steps of collagen homeostasis
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
during maturation phase ___ is replaced by \_\_\_
type III collagen Type 1 collagen
92
during the maturation phase of wound healing the wound will increase in strength by \_\_\_
Collagen organization Cross linking of collagen
93
collagen synthesis can not take place during \_\_\_
hypoxia, fibroblasts are oxygen sensitive healing is energy dependent- proliferative phase has increased metabolism and protein synthesis
94
radiation therapy causes \_\_\_
fibroblast defects are the central problem in thehealing of chronic radiation injury
95
what medication can decrease wound healing
**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
what will glutamine do to wound healing?
Enhance actions of lymphocytes, macrophages and neutrophils
97
what will glycine do to wound healing?
Inhibitory effect on leukocytes, might reduce inflammation related tissue injury
98
what will zinc do to wound healing
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
regeneration vs healing
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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