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BSNC 3000 > Module 2 - Inflammation & Osteoarthritis > Flashcards

Module 2 - Inflammation & Osteoarthritis Flashcards

1
Q

Vascular stage of inflammation

A

cellular injury –> rls of inflammatory cytokines
blood vessels dilate (erythema)
increased hydrostatic pressure –> edema
increase in vascular permeability (endothelial cells contract causing intercellular gaps) –> allow escape of WBCs, proteins etc into interstitial space
inflammatory cytokines & mechanical compression –> pain

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2
Q

Cellular phase of inflammation

A

adhesion & margination
transmigration
chemotaxis
activation & phagocytosis

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3
Q

Adhesion & margination

A

margination = accumulation of WBCs
blood flow slows
endothelial cells express cell adhesion molecules (selectins & integrins)
WBC’s roll & adhere to endothelium

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4
Q

Transmigration

A

endothelial cells separate –> intercellular gaps

WBCs form pseudopods and squeeze thru endothelium

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5
Q

Chemotaxis

A

macrophages release chemokines (proteins) that attract other WBCs to site of inflammation

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6
Q

Neutrophils timeline

A

arrive to site of injury wi 90 minutes

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7
Q

Macrophage timeline

A

arrive to site of injury wi 24 hrs

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8
Q

Function of inflammation

A

eliminate initial cause of cell injury
remove necrotic tissue & debris (prepare area for healing)
initiate healing
initiate immune response

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9
Q

Consequences of inflammation

A

pain (d/t swelling –> mechanical compression)
loss of function
swelling –> can impair blood flow
complications of chronic inflammation (scarring)
excessive inflammation –> autoimmune response

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10
Q

Types of synovial joints

A 
pivot (C1 & C2)
hinge (elbow)
ball & socket (hip/shoulder)
condyloid (radius & carpal bone)
saddle
plane (tarsal bones)
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11
Q

Synovial anatomy

A

joint cavity + synovial fluid
synovial membrane
articular capsule
articular cartilage (hyaline)

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12
Q

Articular cartilage

A

hyaline cartilage that covers the surface of articulating bone
decreases friction, shock absorption

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13
Q

Synovial membrane

A

inner lining of the joint capsule

secretes synovial fluid (lubricating medium)

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14
Q

Joint (articular) capsule

A

connective tissue layer that unites bones & encloses joint cavity

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15
Q

Joint cavity

A

space between articulating bones containing the synovial fluid
allows for free joint movement

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16
Q

Ligaments

A

connective tissue joining bones together

provide joint stability

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17
Q

Tendons

A

connective tissue joining bone & muscle

allow for movement when muscles contract

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18
Q

Bursae

A

fluid filled sacs that reduce friction

located in areas wehre skin, ligaments, muscles or tendons rub against each other (ex: knee)

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19
Q

Menisci

A

fibrocartilage discs found b/w articulating bones

helps to align bones, smooth movements, provide cushioning

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20
Q

Inflammation therapy

A 
RICE (raise, ice, compress, elevate)
NSAID
salicylate (aspirin)
acetaminophen (tyenol)
corticosteroids (prednisone)
antihistamines
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21
Q

Cell-derived inflammatory mediators

A 
histamine (mast cells)
prostaglandins
leukotrienes
cytokines
serotonin
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22
Q

Plasma-derived inflammatory mediators

A

kinin system
complement system

present in plasma

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23
Q

Location of histamine

A 
preformed granules located in mast cells --> immediate, transient response
key mediator of allergic reaction
located in:
airways 
skin 
GI tract
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24
Q

Function of histamine

A

vasodilation, vascular permeability
nasal congestion
bronchoconstriction, increased mucus production (increase goblet cells)
pruritus, hives
stim parietal cells –> increase gastric acid production. impaired absorption (increased motility) & intestinal narrowing
brain –> wakefulness

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25
1st generation H1 antihistamines
ex: diphenhydramine (benadryl) anticholinergic side fx cross BBB --> sedative fx
26
2nd generation H1 antihistamine
ex: ceterezine, loratadine more selective to H1 receptors do not readily cross BBB --> less sedation
27
H2 antihistamines therapeutic fx
parietal cells = H2 receptors decrease stomach acidity (reduce acid secretion) reduce gastric volume (reducing secretions) treat GERD treatment of peptic ulcers
28
Phospholipase A2
intracellular enzyme that releases arachidonic acid from membrane phospholipids
29
Low dose aspirin
high affinity for COX-1 pathway | used as an antiplatelet medication for coagulation disorders
30
High dose aspirin vs ibuprofen
high dose aspirin rarely used to treat pain as it causes severe side fx ibuprofen is preferred as it works as an antipyretic & analgesic with less side fx
31
COX-1 prostaglandins
housekeeping enzymes gastric protection (increase mucus production, decrease acid secretion, increase gastric blodo flow) increase renal blood flow & GFR increase platelet aggregation (hemostasis)
32
COX-2 prostaglandins
``` vasodilation fever pain decrease platelet aggregation (thrombolysis of inappropriate clots) increase Na+ & water excretion ```
33
Local fx of cytokines
increase vascular permeability enhance leukocyte recruitment activate macrophages/lymphocytes
34
Systemic fx of cytokines
fever, fatigue, decreased appetite neutrophilia increase production of acute phase proteins
35
What makes cartilage resilient?
proteoglycans
36
Proteoglycans
core protein with polysaccharide chains | bind tightly with collagen in the ECM
37
How is cartilage nourished
cartilage is avascular compression --> squeezes fluid out of cartilage proteoglycans pull fluid/nutrients back into cartilage
38
Mechanisms of proteoglycan loss
``` aging inflammatory cytokines (IL-1) --> activate enzymes that break down cartilage/proteoglycans ```
39
Primary OA RF
age genetics female sex
40
Secondary OA RF
``` joint injury joint overuse obesity congenital skeletal deformities neurologic disorders neuromuscular disorders hemophilia (bleeding in joints) ```
41
Pathogenesis of OA
``` erosion of articular cartilage subchondral sclerosis formation of subchondral cysts formation of bone osteophytes secondary inflammation ```
42
Synovitis
inflammation of the synovial membrane
43
Subchondral cysts
synovial fluid enters into cracks in the articular cartilage forming cysts increase pressure --> pain
44
Bone osteophytes
bone overgrowths that occur at the edges of articulating surfaces reduce range of motion, cause pain, deformities
45
Subchondral sclerosis
cartilage erosion --> exposes bone increasing bone remodeling thickens bone --> increase friction causing pain
46
Joint mice
parts of the cartilage break off --> synovial membrane | induce secondary inflammation
47
Synovium components
``` connective tissue blood vessels lymphatic vessels type a cells type b cells ```
48
Type A cells
clear cellular debris in synovial cavity | resident macrophages
49
Type B cells
produce synovial fluid
50
Eburnation
exposure of bone caused by degradation of articular cartilage increase friction of bone-bone causes polished appearance
51
Which joints are commonly affected by OA?
weight-bearing joints ``` hips lower back knees neck? hands/feet ```
52
Consequences of OA
``` joint pain joint stiffness decreased mobility decreased ability to do ADL's depression decreased quality of life impaired sleep fatigue joint deformities --> altered self esteem ```
53
Mild OA symptoms
joint pain <30 min. alleviated with rest joint stiffness crepitus
54
Crepitus
popping, cracking sound in a joint
55
Moderate-Severe OA
``` joint pain > 30min at rest & with movement joint stiffness joint enlargement --> osteophytes, joint capsule enlargement decreased ROM, ADL's, mood disturbances muscle weakness (atrophy, inflammation, joint instability) ```
56
Inflammation & Soft Tissue
over time, OA affects the ENTIRE joint including soft issues causes enlargement of the joint capsule causes weakening of the ligament/menisci --> tears contributes to joint instability
57
Pathophysiology of Mild OA
cartilage erosion bone friction subchondral sclerosis pain w/ movement
58
Pathophysiology of Moderate-Severe OA
``` worsening cartilage erosion & friction osteophytes bone cysts secondary inflammation pain @ rest ```
59
Non-pharmacological OA treatment
``` topical capsaicin cream physical activity (PT, OT) moderate activity strength training rest periods glucosamine/chondroitin sulfate supplements weight loss splints/braces/orthopedic devices assistive devices activity/work modification hot/cold therapy ```
60
Pharmacological OA treatment
``` NSAIDs acetaminophen salicylate opioids (severe pain) intra-articular steroidal injections viscosupplementaiton (hyaluronic acid injection) joint surgery ```
61
Rheumatoid arthritis S/S
autoimmune disorder --> primary inflammation affects symmetrical joints distal --> proximal S/S of systemic inflammation (fever, fatigue, anorexia, malaise) warm, boggy joints (d/t inflammation) pain >30 min
62
OA S/S
asymmetrical joints pain <30 min (worse in AM/PM) alleviated with rest crepitus joint enlargement (subchondral sclerosis, osteophytes, joint capsule thickening)
63
What age does OA occur?
> 40-50 yo
64
What age does RA occur?
any age | usually 30-50 yo
65
Causes of post-op inflammation
``` surgical wound infection (UTI, pneumonia, SSI) cellulitis DVT/PE acute MI stress ulcers pancreatitis ```

BSNC 3000 (11 decks)

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