osteoporosis, osteoarthritis, rheumatoid arthritis Flashcards
what is the issue with osteoporosis
- Low bone mass
- Porous bone–the dev of cracks and holes. When bone is porous it cant bear wt.
- Bone is fragile leads to possibe fx?
what is being lost with osteoporosis
how is it helpful to think of osteoporosis
Osteoporisis youre losing matrix, the cells are still there
• Can think of tis as bone atrophy, losing bone mass. Mass generally means wt but for us we are looking at compsoiton of bone.
what kind of actions might cause fx for osteoporotic pt
When fragile the bone can fx with minimal stress eg sitting standing walking
bone remodelling pg 1442
what is bone remodelling and which general steps are involved
bone remodelling is a process of skeletal maint once skeletal growth id complete
it takes place in. the osteons of mature bone and consists of bone resorption by osteoclasts followed by
bone formation by osteoblasts. Bone remodelling is controlled by cytokines and growth factors.
what is mature bone made up of
what changes occur within the bone
osteons or units of oncentric lamella and the haversian canal they surround
bone resorption by osteoclasts followed by bone formation by osteoblasts. this takes 4 months
bone resorption
osteoclasts are activated by osteoblasts releasing mediators they then remove components in a tunnel like space in osteon. From this process the osteoblasts are attracted
what is osteoid
bone formation
the organic matrix secreted by osteoblasts
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what is the etiology of osteoporosis
- Ageing—As we age we tend to remove more than we deposit. This isn’t a direct correlation
- Genetic predisposition-peak bone mass (v important aspect of et)
- Endocrine changes—we saw this clearly in BPH. For women reaching menopause they stop E production. E is supportive of bone. It limits minimizes the activity of osteoclasts. Osteoblasts support growth
what are the risks of osteoporosis
• 2 major risks
o Low peak bone mass—
• Post menopause (inc inc bone loss) major risk factor for women
low PBM as a risk of osteoporosis
what analogy was used
graph with bone mass and age on axes. At age 30 you have reached peak bone mass. Sometime after that we begin to lose bone mass. In earlier stages bone remodelling.At PBM we reach balance. On young side there is pos balance if older theres neg balance
Analogy: theres person working and depositing money for retirement. They are working until age 30. When they stop working they have the amount of $ in account (PBM). Then after retirement they are using their $
what could inc peak bone mass
Pos lifestyle with activity, diet then you can maint the healthy bone mass for longer period of time.
patho of osteoporosis
when is approx PBM?
- Peak bone mass at around 30yrs–then loss begns
- Longitudinal bone growth stops at around 20y
- Imbal bet formation and resorptio
- High bone loss post menopause
- Architectural changes–ext looks normal but int may be holes. If you were to look inside histologically youd see alt in lamellae lacunae etc
- Micro damage sets in
how does bone growth progress? long bones?
the long bone keeps growing until the epiphyseal plate fuses. This usually happens a few yrs after puberty. The bone will inc in diameter but wont elongate
what is gen the 1st mnft of osteoporosis
• Usually silent until fx–it progresses silently although we know it is happening. When a bone breaks they’ll do xray if advanced youc an see it on xray.
o Acute, severe pain
mnft of osteoporosis
• Usually silent until fx Acute, severe pain • Damage to vertebrae Change in stature—(dec height) • Distorted spine Breathing problems
(nutrition d/t poor dentition)
• (if you take maxilla and mandible then the implantation of teeth into the jaw isn’t competent anymore. Their dentition is affected. They no longer want to eat certain things which affects nutrition and metb)
dx of osteoporois
• xray (late stages)–This will initiate with fx
• bone density scan—were looking at absorption and transmission of light. The T score ranges from 1-2.5. The lower the number the greater the osteoporosis
-the 3 gen areas they do this in are:
o 1=lumbar spine
o 2=radius
o 3=Neck of the femur
tx of osteoporosis
unfortunately there isnt much you can do
- Prevent fractures–When you have atrophied bone it wont heal easily..
- Pain and disability–These pts will have lg amount of pain. The force is applied to muscle and the muscles deviate the force to the bone
- Wt bearing activity—promotes bone remodelling
- Antiresorptive agents (osteoclasts)
- Anabolic agents (osteoblasts)
- Adequate protein, Ca and vitamin D—maybe look these up?
whats touching what in a joint, what else is in there?
bones have articulating cartilage which is damaged (bone doesn’t make contact with bone) in bet the cartilage there is synovial fluid.
when theres cartilage damage can it be repaired or replaced?
You cant replace cartilageerosion of the bone. When cartilage is injured and damaged it is diff to repair.
is osteoarthritis mostly due to inflammatory damage or wear and tear
not just degen change
some inflm occurs but it DOESNT cause the primary damage
what is osteoarthritis
where does it occur first?
what occurs?
disease course
• Degen joint disease
Loss of cartilage and subchondral bone
• Tends to occur initially in wt bearing joints. As it progresses it affects smaller joints as well. This is opposite of rheumatoid arthritis
• Wt bearing joints
• Usually non inflm damage–this isn’t considered to be an inflm disease. The inflm isn’t what causes the primary damage!!!!
is the progresion of osteoarthritis slow or fast?
• Slow progression—a young person could injure a joint with repetitive motion (this would be secondary to some form of injury)
what are the tow forms of osteoarthritis
primary and secondary
possible et of primary osteoarthritis
• Primary: idiopathic?
Wear and tear with ageing
• Genetic predisposition?— there are some genes that assist in cartilage maintenance and repair of cartilage.
o Easier cartilage damage and poor repair?
et of secondary osteoarthritis
• Secondary: injury, obesity etc—there is also metb link in terms of the joints themselves which isn’t clearly known
patho of osteoarthritis
• The chondrocytes maint cartilage
• Articular cartilage
o Smooth (less friction), wt bearing—there is also synovial cartilage
o Dissipates force to bone
• Compostion and properties of cartilage change->(chondrocytes rel-interleukin and TNF) cytokines-> proteases-> destr of cartilage
• Chondrocyte damage->impaired ability to heal cartilage
• Cartilage deteriorate->unprotected bone (bone upon bone)->sclerosis of bone
• Cysts and fissures appear as fluid enters cracks in bone
• Osteophytes form->joint enlarges and deforms–the second attempt is to form new bone. They are projections and not normal
why does the composition and property of cartilage change in OA
d/t the genetic change
what are the ways the body compensates to protect the bone?
helpful?
—the body attempts to protect body by solidifying the bone but it isn’t helpful, you need the articulating surface
–the second attempt is to form new bone (osteophytes form which enlarge and deform joint)
fig 59.6. this is like flow chart for osteoarthritis
mechanical injury leads to what?
mech–>chrondrocyte response–>cytokines->proteases–>destruction of joint str (which also leads back to chondrocyte response)
orrrrrr the proteases–>loss of smooth cartilage surface–>development of surface cracks–>destruction of subchondral bone–>osteophyte formation
fig 59.5 what normally occurs to articular cartilage when carrying a load?
what occurs when this normal process doesnt occur?
the joint normally underoes deformation of articular cartilage and subchondral bone to maximize the contact area and spread the force of the load.
if it doesnt deform with load the stress is concentrated and the joint breaks down
another longer version of bone remodelling
which hormones begin bone remodelling?
what signals what to start bone remodelling?
o Bone remodelling occurs in osteons, the length of one sequence takes approx 4 months
o In elderly bone resorption and formation are no longer perfectly coupled and bone mass is lost
o Parathyroid hormone and calcitonin are involved with initiating the bone remodelling. They affect osteoblasts more, when the osteoblast gets this signal it releases RANKL mediator to signal osteoclast to begin bone remodelling
o Osteoclasts begin to remove in/organic components to create a tunnel like space in osteon
o Factors are released in this process that attrack osteoblasts which deposit osteoid on the wall of the osteon canal until the relative proportions of the orig osteon are reached
o The osteoblast releases RANKL which in combo with osteoprotegerin promotes osteoclast differentiation and proliferation
o This system provides tight coupling of bone formation and resorption
mnfts of osteoarthritis
- Initial: non localized aching pain
- Later: activity related wt bearing joint pain
- Crepitus
- Stiff, inflm joint
- Bones work in concert with muscles (they will stiffen and go into spasm) present with msksltl pain
what is crepitus
a grating sound or sensation produced by friction between bone and cartilage or the fractured parts of a bone.
what is the progression from initial to late symptoms
—as the condition progresses the pain inc and is r/t activity and use of the joint…ends up being activity related wt bearing joint pain
what causes the stiffness of the joint
When they use the joint it hurts but when they don’t move it it stiffens.
dx of osteoarthritis
- Hx, px
- Xray not always useful—if there is severe damage you can see. May indicate inflm change, narrowing of joint
- Labs—done largely to exclude other forms of arthritis particularly rheumatoid arthritis. also Exclude septic arthritis.Look at CRP, ESR etc etc.
tx of osteoarthritis
what is the first choice? what is it good for?
other tx options?
what is curative?
- Monotherapy prn
- Tylenol (1st choice)—good for initial stages
- Cox 2 inhibitors
- Severe: intra articular injection—they inject directly into joint.
- Rehabilitative—want to maximize usage of joint through exercise, wt loss
- Sx—this is only curative approach
what is Cox 2 and what does it do
—cyclooxygenase-an Es that does two things 1. It enhances inflm 2. Leads to formation of prostaglandin (which is involved in mediating pain)
what is rheumatoid arthritis?
who is it common in?
which joints are affected here?
• It is a systemic disease. 80% occurs in women because it is autoimmunity. It is a connective tissue disease
• Chronic autoimmune CT disease
o Inflm deformed synovial joints
–Here the smaller joints are affected more, as it progresses it will affect wt bearing joints
et of rheumatoid arth
Et
• Multifactorial (complex trait)
• Viral trigger—Eppstein Barr virus is strongly involved
-Genetic predisposition (HLA genes)
patho of rheumatoid arthritis
• Alt T cell response->targets synovial membr (in the joint….this is before the cartilage)->inflm and joint damage
• Alt B cells->Abs prod (rheumatoid factors (RF))->target tissues
• RF form ICs->deposit in synovial membrane->inflm
• Repeated inflm->deformity –unlike when we use the joint and it deforms physiologically
• Pannus
-Releases detructive Es—
-Has damaging inflm cells –(within the pannus)
-Decreases joint mobility
are rheumatoid factors reliable inicators of rheum arthritis
–In most pts you will be able to detect RF. But you ant really on this
what is a pannus
(vascular, granulation tissue)—the joint has limited space. Granulation tissue is a form of vascular tissue. Youre attempting to bring about healing itn the joint.
59.1 this is another example of the patho of rheumatoid arthritis which I copied from flow chart
genetic predisposition (HLA type) plus trigger–>T cell IR–>RF Ag/IgG interaction–>complement fixation–>inflm (this can either lead to angiogenesis in synovium–>synovial proliferation->pannus invasion orrr) the inflm–>recruitment of inflm cells–> Es and prostaglandins–>destr of articular cartilage and underlying bone…… third thing that impacts this articular cartilage and underlying bone is the cytokines from the Tc cells
is rheumatoid arthritis a joint disease
no it is a connective tissue issue
mnfts of rheumatoid arthritis
• Articular and extra articular–Often RA is confused as just joint disease
• Subtle onset
o malaise, low grade fever—if during the viral trigger these r/t the virus
• increasing fatigue
• AM joint pain
• Stiffness after inactivity
• Non articular
Heart, blood vessels, skin, lungs, eyes—vision and ocular problems. This is systemic
why does a pt have joint pain in morning with RA
• AM joint pain—because you don’t utilize the joints at night
after what does joint pain appear
inc fatigue—only after this do they present with joint issues
around what age does RA often set in
(Happens often at fairly early age around 30)
dx of RA
- Hx, px–Not difficult. Will involve exhaustive workup
- X-ray, labs—the xray isn’t revealing in earlier stages. The labs aren’t too exclude too much, you are wanting to test the RF (not all come through positive even though they have it). There is whole series of antibodies measured eg antinuclear Abs to exclude other autoimmune problems
tx of rheum arth
• Limit progression
• Pain (eg meloxicam) –they may instead use naprosym (or naproxen)
• Start with plaquenil
• Usually combination therapy eg
o Sulfasalazine and methotrexate (CBC, liver Es, and creatinine monthly)–(theyd stop Plaquenil and use it instead)— Methotrexate is anti folate. The labs would be standing order
what is plaquenil
—anti inflm, and immunomodulatory. A problem with Plaquenil is that it deposits in the eyes and causes ocular issues
(eye exam q6-12months)
sulfasalazine as tx of RA
sulfasalazine is also used for anti inflm and immunomodulator.
what is methotrexate ra
Methotrexate is anti folate
