Module 4 - NR 565
Osteoarthritis rate of onset
slow (years)
OA prevalence based on gender:men 1:1
age of onset of OA greater then 40 years
A lot of OA joints are affected. hands (DIP), large joints that can bear weight (hips, knees) OA
joint symptoms
Pain, bony enlargement
Inflammation from OA none or mild, local
OA the degree of stiffness in the morning joints usually less then 30 minutes
OA joint pattern
asymmetry or symmetry OA ESR
normal
OA synovial fluid
mild leukocytosis
OA systemic symptoms
none
Rate of onset of RA rapid (weeks to months)
RA incidence based on gender (women:men)
3:1
age of onset of RA juvenile or adult (35-50)
RA joints commonly affected
small joints of hands (MCP, PIP), feet
RA inflammation
local and systemic
RA the extent of stiffness in the morning
usually more than 60 minutes RA joint pattern
symmetric
RA ESR
elevated
RA synovial fluid
leukocytosis, a little hazy Systemic symptoms of RA yes
cytokines that cause joint damage factor tumor necrosis IL-1
IL-6
IFN-y
platelet-derived growth factor
granulocyte- macrophage colony- stimulating factor
treatment of RA is directed toward what four things
1. reducing symptoms like pain, stiffness, and inflammation 2. preserve joint mobility and
function 3. minimize systemic involvement
, 4. halt the progression of disease There are three types of RA drugs. NSAIDs
glucocorticoids
DMARDs
NSAIDs in RA
provide rapid, symptomatic relief of inflammation and pain
first generation NSAIDs
Cox-1 & Cox-2
Aspirin
ibuprofen
meloxicam
naproxen
NSAIDs of the second generation Inhibitors of COX-2 (Celebrex) glucocorticoids provide
quick relief from symptoms slow disease progression
can cause toxicity issues
glucocorticoids
Hydroxycortison, prednisone, triamcinolone, dexamethasone, beclomethasone. - decreases the
production of leukotrines and prostaglandins by inhibiting phospholipase A2and expression of
COX - 2. Used clinically in addisons disease, inflammation, immune suppression, asthma.
toxicity includes iatrogenic cushings syndrome - buffalo hump, moon facies, truncal obesity,
muscle wasting, thin skin, easy bruisability, osteoporosis, adrenocortical atrophy, peptic ulcers,
diabetes (if chronic). adrenal insufficiency when drug stopped abruptly after chronic use.
disease-modyfing anti rheumatic drugs (DMARDs)
reduce joint destruction and slow disease progression
interfere in the immune and inflammatory process
Three types of DMARDs 1: nonbiologics=immunosuppressants (conventional)
2:biologics=mabs
3: targeted= only after others
conventional DMARDs
Methotrexate
Leflunomide
Sulfasalazine
Hydroxychloroquine
biologic DMARDs
-Immunosuppressive drugs that target specific components of the inflammatory process
-Usually used in conjunction with methotrexate TNF antagonists (Entanercpt/Enbrel)
Rituximab (Rituxan)
Abatacept from Orencia Tocilizumab (Actemra)
Anakinra (Kineret)
targeted DMARDs
block precise pathways inside immune cells
Tofacitinib
Baricitinib
What is the first-line treatment for OA
NSAIDs
Osteoarthritis rate of onset
slow (years)
OA prevalence based on gender:men 1:1
age of onset of OA greater then 40 years
A lot of OA joints are affected. hands (DIP), large joints that can bear weight (hips, knees) OA
joint symptoms
Pain, bony enlargement
Inflammation from OA none or mild, local
OA the degree of stiffness in the morning joints usually less then 30 minutes
OA joint pattern
asymmetry or symmetry OA ESR
normal
OA synovial fluid
mild leukocytosis
OA systemic symptoms
none
Rate of onset of RA rapid (weeks to months)
RA incidence based on gender (women:men)
3:1
age of onset of RA juvenile or adult (35-50)
RA joints commonly affected
small joints of hands (MCP, PIP), feet
RA inflammation
local and systemic
RA the extent of stiffness in the morning
usually more than 60 minutes RA joint pattern
symmetric
RA ESR
elevated
RA synovial fluid
leukocytosis, a little hazy Systemic symptoms of RA yes
cytokines that cause joint damage factor tumor necrosis IL-1
IL-6
IFN-y
platelet-derived growth factor
granulocyte- macrophage colony- stimulating factor
treatment of RA is directed toward what four things
1. reducing symptoms like pain, stiffness, and inflammation 2. preserve joint mobility and
function 3. minimize systemic involvement
, 4. halt the progression of disease There are three types of RA drugs. NSAIDs
glucocorticoids
DMARDs
NSAIDs in RA
provide rapid, symptomatic relief of inflammation and pain
first generation NSAIDs
Cox-1 & Cox-2
Aspirin
ibuprofen
meloxicam
naproxen
NSAIDs of the second generation Inhibitors of COX-2 (Celebrex) glucocorticoids provide
quick relief from symptoms slow disease progression
can cause toxicity issues
glucocorticoids
Hydroxycortison, prednisone, triamcinolone, dexamethasone, beclomethasone. - decreases the
production of leukotrines and prostaglandins by inhibiting phospholipase A2and expression of
COX - 2. Used clinically in addisons disease, inflammation, immune suppression, asthma.
toxicity includes iatrogenic cushings syndrome - buffalo hump, moon facies, truncal obesity,
muscle wasting, thin skin, easy bruisability, osteoporosis, adrenocortical atrophy, peptic ulcers,
diabetes (if chronic). adrenal insufficiency when drug stopped abruptly after chronic use.
disease-modyfing anti rheumatic drugs (DMARDs)
reduce joint destruction and slow disease progression
interfere in the immune and inflammatory process
Three types of DMARDs 1: nonbiologics=immunosuppressants (conventional)
2:biologics=mabs
3: targeted= only after others
conventional DMARDs
Methotrexate
Leflunomide
Sulfasalazine
Hydroxychloroquine
biologic DMARDs
-Immunosuppressive drugs that target specific components of the inflammatory process
-Usually used in conjunction with methotrexate TNF antagonists (Entanercpt/Enbrel)
Rituximab (Rituxan)
Abatacept from Orencia Tocilizumab (Actemra)
Anakinra (Kineret)
targeted DMARDs
block precise pathways inside immune cells
Tofacitinib
Baricitinib
What is the first-line treatment for OA
NSAIDs
