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Patho 1 > Chap 3- Inflammation and repair > Flashcards

Chap 3- Inflammation and repair Flashcards

1
Q

inflammation

A

response of vascular tissue to infection and damage

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2
Q

causes of inflammation

A
  • infections
  • tissue necrosis
  • foreign bodies
  • immune reactions
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3
Q

inflammatory cells

A
  • neutrophils
  • eosinophils
  • basophils
  • mast cells
  • phagocytes
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4
Q

neutrophils

A
  • main fn is phagocytosis
  • internalize pathogen and destroy it
  • has antimicrobial factors
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5
Q

eosinophils

A
  • eradicate parasites
  • mainly found in GI tract
  • trigger mast cells which releases histamines
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6
Q

basophils

A

-circulating cells
- involved in allergic rxn
- have IgE receptors
release histamine and prostaglandins

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7
Q

mast cells

A
  • live in connective tissue close to blood vessels
  • involved in immediate allergic rxn
  • main source of histamines
  • receptors for IgE
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8
Q

monocyte

A
  • type of phagocyte
  • precursor for macrophages
  • found in blood cell
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9
Q

macrophage

A
  • once monocyte reaches target tissue is called macrophage
  • type of phagocyte
  • derived from hematopoietic stem cells in bone marrow
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10
Q

steps of phagocytosis

A
  1. recognition and attachment-
    pathogen attaches to receptor
  2. engulfment
  3. killing by ROS or degradation by lysosomes
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11
Q

How are ROS derived?

A
  • can be from leukocytes after phagocytosis

- exposure to chemokines, immune complexes, or microbial products

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12
Q

Effect of ROS

A
  • endothelial cell damage -> increased vascular permeability

- injury to multiple cell types by oxidative stress

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13
Q

mediators of inflammation

A
  • “middle man”
  • initiate and regulate inflammation
  • either secreted by cells or made from plasma proteins
  • short lived
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14
Q

Histamine

A
  • inflammatory mediatior
  • main source= mast cells
  • cause vasodilation, increased vascular permeability
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15
Q

prostaglandins

A
  • inflammatory mediator
  • main source= mast cells
  • cause vasodilation, pain, fever
  • generated by COX
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16
Q

leukotrienes

A
  • inflammatory mediator
  • main source= mast cells
  • cause increased vascular permeability, involved in vascular/smooth muscle response, leukocyte recruitment
  • generated by lipoxygenase
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17
Q

Cytokines (TNF, IL-1)

A
  • inflammatory mediator
  • mains source= macrophages, helper t cells
  • local action= endothelial activation
  • systemic action= fever
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18
Q

chemokines

A
  • inflammatory mediator
  • main source= leukocytes, activated macrophages
  • cause chemotaxis
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19
Q

Platelet- activating factor (PAF)

A
  • inflammatory mediator
  • main source= leukocytes, mast cells
  • cause platelet aggregation and degranulation
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20
Q

complement system

A
  • inflammatory mediator
  • main source= plasma produced in liver
  • action- direct target killing (via membrane attack complex)
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21
Q

3 functions of histamine

A
  • vasodilation in arterioles
  • increased permeability of venules
  • smooth muscle contraction
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22
Q

serotonin

A
  • same effect as histamines

- comes from platelets

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23
Q

arachidonic acid metabolites

A
  • lipid mediators produced from phospholipid bilayer of plasma membrane
  • types: prostaglandins, leukotrienes, lipoxins
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24
Q

lipoxins

A
  • generated by lipoxygenase

- suppress inflammation by inhibiting recruitment of leukocytes

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25
cytokine
-broad umbrella term for proteins that mediate and regulate inflammatory response
26
role of chemokines
- type of cytokine - chemotaxis - guide neutrophil to move towards invader
27
inflammatory reaction's sequence of events
1. recognition by receptors 2. recruit leukocytes and plasma proteins 3. remove dead cells/ bacteria/ pathogen etc. 4. regulate inflammatory response 5. resolution/repair
28
TLRs
- toll like receptors - recognize pathogen in or outside of cell recognize pathogen-associated molecular patterns (PAMPs) which stim release of inflammatory mediators
29
DAMPS
- damage-associated molecular patterns | - recognize endogenous stimuli
30
Function of complement system
- opsonization and phagocytosis - inflammation - cell lysis by forming membrane attack complex (MAC)
31
what are the complement proteins involved in inflammation?
C3a and C5a
32
What does C3b do?
it is like a flag, marks pathogen to be eaten
33
types of pathways that the complement system can join together to function
- classical pathway- binds to antibody, used in adaptive immunity - lectin pathway- mannose that binds to lectin, used innate immunity - alternative pathway- used in innate immunity
34
major components of acute inflammation
- vasodilation and increased blood flow - increased permeability and leukocyte migration - emigration and activation of leukocytes
35
what is blood caliber?
diameter of blood vessel gets increased by vasodilation
36
what is stasis of blood flow?
movement of RBC slows down
37
what are vascular reactions to acute inflammation?
- vasodilation via histamines - stasis of blood flow - neutrophils accumulate along epithelium - increased permeability of vessels
38
what do lymphatic vessels and lymph nodes do during inflammation?
- filter extravascular fluids, become engorged | - want to direct this extra fluid towards the circulation and out of extracellular space
39
reactions of leukocytes in inflammation
1. rolling and adhesion to endothelium (selectins and integrins) 2. diapedesis- get out of blood vessel, results in vascular congestion 3. migration in the tissues toward a chemotactic stimulus
40
allergy
excessive inflammatory response
41
autoimmune disease
misdirected inflammatory response against body's own tissues
42
possible outcomes of acute inflammation
- resolution- not too much damage so tissues regenerate/repair - fibrosis- loss of function - chronic inflammation- occurs when injury persists and cannot heal properly
43
chronic inflammation
- inflammation lasting longer than a few weeks - caused by persistent infection, hypersensitivity diseases, prolonged exposure to toxic substance - phagocytes and lymphocytes found with chronic inflammation
44
role of macrophages in chronic inflammation
- phagocytic function - initiate tissue repair - participate in scar formation and fibrosis - secrete TNF, IL-1 and ROS causing inflammation and tissue injury - present antigen to T lymphocyte
45
role of lymphocytes in chronic inflammation
- when lymphocytes activated inflammation is persistent and severe
46
relationship of lymphocytes and macrophages
- macrophages activate lymphocytes - lymphocytes activate macrophages both cause chronic inflammation
47
granulomatous inflammation
- form of chronic inflammation | - necrosis in center, lymphocytes, macrophages, epithelioid cells, macrophages that have fused together
48
types of granulomas
- foreign body granulomas | - immune granulomas
49
systemic effect of inflammation
- fever caused by pyrogens - acute- phase proteins made in liver - leukocytosis- increased WBCs
50
what are acute-phase proteins?
- synthesized in liver - c- reactive proteins attach to microbial cell wall, act like flag for complement system - fibrinogen- attach to RBC and makes stack of RBC
51
what is tissue repair?
rebuilding of tissue architecture and function after injury
52
mechanisms of tissue repair in mild tissue injury
- proliferation of surviving cells | - maturation of tissue stem cells
53
tissue repair in severe injury
- results in scar formation | - excessive amount of collagen and extracellular material deposited
54
labile tissues
cells proliferate throughout life | i.e. skin
55
stable tissues
proliferation capacity is limited, if enough stimulation then they can go through the cell cycle i.e. the liver
56
permanent tissues
tissue cannot divide in postnatal life so damage is permanent i.e. brain
57
cell proliferation
tissue goes through cell cycle, makes copies of itself
58
fibroblasts
make collagen
59
what are the steps in scar formation?
1. inflammation for 6-48 hours, macrophages are major players 2. cell proliferation for up to 10 days- epithelial cells respond to GF, angiogenesis occurs, fibroblasts function 3. remodeling of connective tissue starts 2-3 weeks after injury- scar tissue
60
what is the difference between fibrosis and scarring?
- fibrosis- better used for internal organs | - scarring- usually for skin or wound healing
61
Systemic factors effecting tissue repair
- nutritional status - metabolic status - circulatory status - hormones
62
Local factors effecting tissue repair
- size, location, and type of wound - infection** - mechanical forces - foreign bodies
63
venous leg ulcer
- chronic wound | - due to lack of oxygen and nutrients to extremities
64
arterial ulcer
- chronic wound | - usually caused by atherosclerosis, reduced blood supply
65
pressure sore
- chronic wound | - mechanical force of tissue against bone, area becomes ischedmic
66
hypertrophic scars
excessive collagen accumulation forms raised scar
67
keloid
progression beyond original area of injury
68
exuberant granulation
blocks reepithelization, excessive amount of granulation tissue
69
contractures
is an exaggerated process that results in wound deformity (common in burn victims)
70
fibrosis
- excessive deposition of collagen - pathologic process - cytokines stim fibroblasts -> collagen and othe ECM protein deposition

Patho 1 (12 decks)

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