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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
Q

1st generation H1 antihistamines

A

ex: diphenhydramine (benadryl)

anticholinergic side fx
cross BBB –> sedative fx

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26
Q

2nd generation H1 antihistamine

A

ex: ceterezine, loratadine

more selective to H1 receptors
do not readily cross BBB –> less sedation

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27
Q

H2 antihistamines therapeutic fx

A

parietal cells = H2 receptors

decrease stomach acidity (reduce acid secretion)
reduce gastric volume (reducing secretions)
treat GERD
treatment of peptic ulcers

28
Q

Phospholipase A2

A

intracellular enzyme that releases arachidonic acid from membrane phospholipids

29
Q

Low dose aspirin

A

high affinity for COX-1 pathway

used as an antiplatelet medication for coagulation disorders

30
Q

High dose aspirin vs ibuprofen

A

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
Q

COX-1 prostaglandins

A

housekeeping enzymes

gastric protection (increase mucus production, decrease acid secretion, increase gastric blodo flow)
increase renal blood flow & GFR
increase platelet aggregation (hemostasis)

32
Q

COX-2 prostaglandins

A 
vasodilation
fever
pain
decrease platelet aggregation (thrombolysis of inappropriate clots)
increase Na+ & water excretion
33
Q

Local fx of cytokines

A

increase vascular permeability
enhance leukocyte recruitment
activate macrophages/lymphocytes

34
Q

Systemic fx of cytokines

A

fever, fatigue, decreased appetite
neutrophilia
increase production of acute phase proteins

35
Q

What makes cartilage resilient?

A

proteoglycans

36
Q

Proteoglycans

A

core protein with polysaccharide chains

bind tightly with collagen in the ECM

37
Q

How is cartilage nourished

A

cartilage is avascular
compression –> squeezes fluid out of cartilage
proteoglycans pull fluid/nutrients back into cartilage

38
Q

Mechanisms of proteoglycan loss

A 
aging 
inflammatory cytokines (IL-1) --> activate enzymes that break down cartilage/proteoglycans
39
Q

Primary OA RF

A

age
genetics
female sex

40
Q

Secondary OA RF

A 
joint injury
joint overuse
obesity
congenital skeletal deformities
neurologic disorders
neuromuscular disorders
hemophilia (bleeding in joints)
41
Q

Pathogenesis of OA

A 
erosion of articular cartilage
subchondral sclerosis 
formation of subchondral cysts
formation of bone osteophytes
secondary inflammation
42
Q

Synovitis

A

inflammation of the synovial membrane

43
Q

Subchondral cysts

A

synovial fluid enters into cracks in the articular cartilage forming cysts
increase pressure –> pain

44
Q

Bone osteophytes

A

bone overgrowths that occur at the edges of articulating surfaces
reduce range of motion, cause pain, deformities

45
Q

Subchondral sclerosis

A

cartilage erosion –> exposes bone increasing bone remodeling
thickens bone –> increase friction causing pain

46
Q

Joint mice

A

parts of the cartilage break off –> synovial membrane

induce secondary inflammation

47
Q

Synovium components

A 
connective tissue
blood vessels
lymphatic vessels
type a cells
type b cells
48
Q

Type A cells

A

clear cellular debris in synovial cavity

resident macrophages

49
Q

Type B cells

A

produce synovial fluid

50
Q

Eburnation

A

exposure of bone caused by degradation of articular cartilage
increase friction of bone-bone causes polished appearance

51
Q

Which joints are commonly affected by OA?

A

weight-bearing joints

hips
lower back
knees
neck?
hands/feet
52
Q

Consequences of OA

A 
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
Q

Mild OA symptoms

A

joint pain <30 min. alleviated with rest
joint stiffness
crepitus

54
Q

Crepitus

A

popping, cracking sound in a joint

55
Q

Moderate-Severe OA

A 
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
Q

Inflammation & Soft Tissue

A

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
Q

Pathophysiology of Mild OA

A

cartilage erosion
bone friction
subchondral sclerosis
pain w/ movement

58
Q

Pathophysiology of Moderate-Severe OA

A 
worsening cartilage erosion & friction
osteophytes
bone cysts
secondary inflammation
pain @ rest
59
Q

Non-pharmacological OA treatment

A 
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
Q

Pharmacological OA treatment

A 
NSAIDs
acetaminophen
salicylate 
opioids (severe pain)
intra-articular steroidal injections
viscosupplementaiton (hyaluronic acid injection)
joint surgery
61
Q

Rheumatoid arthritis S/S

A

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
Q

OA S/S

A

asymmetrical joints
pain <30 min (worse in AM/PM) alleviated with rest
crepitus
joint enlargement (subchondral sclerosis, osteophytes, joint capsule thickening)

63
Q

What age does OA occur?

A

> 40-50 yo

64
Q

What age does RA occur?

A

any age

usually 30-50 yo

65
Q

Causes of post-op inflammation

A 
surgical wound
infection (UTI, pneumonia, SSI)
cellulitis
DVT/PE
acute MI
stress ulcers
pancreatitis

BSNC 3000 (11 decks)

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