Week 2- inflammation Flashcards
1
Q
inflammation
A
coordinated vascular and cellular response of the body to cell injury and cell death
- has protective and curative features
- removal of injurious agent & initiates healing process
2
Q
factors that can initiate inflammation
A
- infection (bacterial, viral, fungal, parasitic)
- trauma/damaged tissue
3
Q
factors that result in inflammation
A
- tissue necrosis, presence of foreign bodies including splinters, dirt, sutures, crystal deposits
- ischemia
- cancer
4
Q
Goals of an inflammatory response
A
- inactivate injurious agents
- breakdown and remove dead cells and other cellular debris
- initiate tissue healing
5
Q
chemical mediators in inflammation process
A
- histamine, bradykinin, prostaglandins
6
Q
cytokines
A
- signaling molecules
- any number of substances such as interferon, interleukin, & growth factors which are secreted by certain cells of the immune system and effect other cells
7
Q
chemokines
A
- tiny protein molecules that form a subfamily of the cell signaling molecules or cytokines
- direct or signal the movement of cells
- attract cells to an area of injury (monocytes/macrophages, T-lymphocytes, eosinophils, neutrophils, mast cells
8
Q
chemokines getting into the cell
A
- floating around, has receptors and is attracted to endothelial lining; has to get through it into interstitial space, chemokine bring structural change so it can squeeze between the cells that make up the lining and to into area of injury
9
Q
Inflammation sign- erythema
A
- vasodilation and increased blood flow
10
Q
inflammation sign- heat
A
- vasodilation and increased blood flow
11
Q
inflammation sign- edema
A
- fluid and cells leaking from local blood vessels into the extravascular spaces
12
Q
inflammation- pain
A
- direct trauma; chemical mediation by bradykinins, histamines, serotonin; internal pressure secondary to edema; swelling of the nerve endings
13
Q
cytokine storm syndrome
A
- inflammatory process wreaks more havoc than the disease itself- can not get the foot off of the accelerator
14
Q
inflammation process- increased vascular permeability
A
- smaller arterioles become “leaky” or permeable
- allow for passage of a protein and cell rich fluid (exudate) into the IS
- allows for accumulation of platelets and neutrophils at site of injury
15
Q
neutrophils (WBC)
A
- key functions of eliminating the offending agent and cleaning up the area
16
Q
leukocytes
A
- lining alveoli, gut
17
Q
diapedesis
A
- epithelial cells stimulated to separate so neutrophils can squeeze into the space into interstitial space
18
Q
WBC count is an important sign of?
A
infection
19
Q
neutropenia
A
- condition where there is a shortage of WBC
- FOCUS ON good hygiene
20
Q
monocytes
A
- circulate in blood
- replenish resident macrophages under normal states
- move to site of injury and differentiate into macrophages and dendritic cells
21
Q
macrophages
A
- engulfs and digests cellular debris, foreign substances, microbes, cancer cells
- langerhans- skin
- kupffer cells- liver
- alveolar macrophage
- microglia- CNS
22
Q
lymphocytes
A
- main type of cell found in the lymph
- produce antibodies
- sub types (natural killer cells, B-cells, T-cells)
- live in bursa an produce B-cells
23
Q
mast cells
A
- found in most tissues of the body (skin, airways, intestine)
- large granules which hold several performed immune mediators
- release ( histamines, serotonin, thromboxane, prostaglandins, leukotriene, platelet activating factor, cytokines, TNF alpha
- allergies
24
Q
How do inflammatory cytokines result in skeletal muscle injury?
A
by activating the ubiquitin- proteasome degradation pathway and enhancing autophagy-lysosome degradation pathway
- cytokines are damaging cause they initiate this process
- inhibit the proliferation and differentiation of myogenic cells thus interfering with normal repair processes
- protein degradation leads to a loss of myofibrillar protein, decreased fiber cross sectional area-> muscle atrophy
- cytokines that stimulate and inhibit inflammation=a balance
- when injury occurs favor pro-inflammatory state
25
RA pathology
- chronic pro-inflammatory disorder
- TNF is culprit
- synovial membrane-> synovial cells multiply in #, influx of leukocytes from the peripheral circulation and synovium becomes edematous
- attract WBC which phagocytize the immune complexes
- release of metalloproteases which degrade cartilage
- inhibits bone formation and stimulates bone resorption
- results in structure called pannus
26
Anti-TNF compounds- biologics
- adalimumab (humira)
- entanercept (enbrel)
- infliximab (remicade)
27
non-TNF biologics
- tocilizumab (actemar)
| - anakinra (kineret)
28
systemic effects of acute inflammation & what are the messengers?
- fever
- somnolence, malaise
- anorexia
- hypotension
- accelerated degradation of skeletal muscle
- increased circulating levels of IL-1, IL-6, TNF and other pro-inflammatory cytokines
29
leukocytosis
- increased white blood cell count
30
leukopenia
- decreased WBC
- viral infections, protozoan, rikettsial, and some bacterial infections
- encountered in patients who are debilitated or immune compromised
31
M1 macrophages
- macrophages that encourage inflammation
- first on scene of muscle injury (0-48 hr)
- pro-inflammatory
- favors tissue cleanup but remember there is always collateral damage
32
M2 macrophages
- macrophages that are anti-inflammatory and encourage tissue repair
- release soluble substances that influence the proliferation, differentiation, growth, repair, and regeneration of muscle
33
parenchymal cells
- cells that form fundamental structure of tissue
34
complete resolution
- normal function returns, clearance of injurious stimuli, clearance of all mediators and acute inflammatory cells, replacement of injured cells with normal functional healthy cells
35
abscess formation
- accumulation of pus in a confined space
- abscess on skin= pustule or pimple
- pus is formed from neutrophils destroyed by macrophages
- often requires draining
36
healing by fibrosis or scarring
- preinjury tissue replaced by connective tissue (fibrosis)
- functioning parenchymal cells are required for normal recovery from injury
- if not available, normal healing does not occur
- if normal tissue cytoskeletal is damaged fibrosis wins!!!!!
37
therapists seek to limit inflammation by
- RICE
- OTCs
- return to play?
- can lead into chronic inflammation
38
progression to chronic inflammation
- happens when the neutrophils and their fast-acting molecular allies cannot remove the noxious agents
- prolong duration of an inflammatory response- weeks to months to years
- characterized by continuous tissue injury w/ongoing attempts at repair
39
MS
- damage to myelin sheath and motor neurons
40
hypersensitivity diseases
- excessive and inappropriate activation of the immune system
- RA, SLE, MS, inflammatory bowel disease, asthma, rheumatic heart disease
41
chronic inflammation arises from
- prolonged/chronic exposure to toxic agents (silca, cholesterol, cigarette smoke)
- Obesity
- chronic stress
- ETOH
42
angiogenesis
- growth of blood vessels
43
granulomatous inflammation
- form of chronic inflammation
- caused by an accumulation of macrophages
- sometimes present with a central abscess
- foreign body: talc, suture, surgical sponges
- TB
- fungal infections
- present in some diseases such as Crohn's
