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Rheumatoid arthritis
Rheumatoid arthritis (RA) is a chronic, systemic inflammatory disorder that may affect
many tissues and organs, but principally attacks flexible (synovial) joints , and it's the
most common persistent inflammatory arthritis, occurring throughout the world and in
all ethnic groups.
Generally, all rheumatic diseases can be local diseases but generally, they have
systemic involvement and RA is one of the common rheumatic diseases; at least, 1% of
people worldwide are affected by RA.
So, RA is a systemic disease, primarily presents as Arthritis -affecting the joints- so the
main problem is arthritis & Other Organs can be involved.
Etiology is not clear, probably Multifactorial [both genetic and environmental factors appear to
be involved], but we know the mechanism of the disease [RA is characterized by infiltration of
the synovial membrane with lymphocytes, plasma cells, and macrophages. CD4+ T cells play a central
role by interacting with other cells in the synovium. Activated T cells stimulate B cells to produce
immunoglobulins including RF, and macrophages to produce pro-inflammatory cytokines. These act on
endothelium, synovial fibroblasts, bone cells and chondrocytes to promote swelling and congestion of
the synovial membrane and destruction of bone, cartilages and soft tissue.] and because of that, we
have more options for treatment. (TNF, iL-1, 6 are important so they create drugs that
block them)
Diagnosis:
-
Typical clinical presentation [joint pain, swelling and stiffness affecting the small
joints of hand, feet and wrist (without swelling, no Dx of RA)]
Rheumatoid factor presence or absence does not make or exclude diagnosis but
positive RF means more extra-articular manifestations and more severe
manifestations [because RF can form immune complexes within the joint and extra articular
tissues, leading to vasculitis.]. In old days, we said that 70% of affected are RF positive
and it was part of the criteria and now its more important in the criteria than
before.
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You have to exclude other diseases that may mimic RA or cause arthritis (other
than RA).
With synovial inflammation, the thickness becomes hundreds of cells. In this case, the
synovium will act as a tumor, it will invade the bone and the cartilage and destruct
them and for that reason, the erosions in RA are lateral on the sides while the inside
damage will be later.
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Anemia*.
Eosinophilia*.
Thrombocytosis*.
Increased levels of alkaline phosphatase, Aspartate amino-transferase, and gammaglutamyl-transferase.
Decreased albumin and pre-albumin.
Elevated erythrocyte sedimentation rate [ESR]*.
Elevated C-reactive protein [CRP]*
Increase ferritin* (ferritin is considered as acute phase reactant; any patient with
anemia & increased ferritin then think of chronic inflammatory disease).
Now, the dr. had moved on to show us different pictures to patients with RA:
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still
relatively
This is metatarso-phalygeal
[MTP] joint, it can be also
affected.
osteoporosis,
The dr. said that hell not comment that much on the X-Ray but if you see X-Ray in
the exam that shows ulnar deviation and damage on the MCP joint, it will be
rheumatic Arthritis, there will be no another question about it.
Differential Diagnosis:
-
Viral syndromes.
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Keratoconjunctivitis sicca.
Uveitis
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The spinal cord may affected because it has synovioum around the odontoid process
and this synovioum may cause damage to the transverse ligament or to the odontoid, if
it causes damage to the ligament, it will cut & cause compression on the spinal cord.
Signs of SC damage:
-
Motor weakness
Jumping legs
<<< When the spinal cord is affected the patient may die! They take him to the
surgery and the anesthetic resident dont know that he has RA and he push the patient
backward with force so the patient has trans-sectional cord and he die on the table!
>>>
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This is the new criteria, and you dont have to remember it.
If you have more than 10 joints involvement then you have at least 1 small joint
because this is a poly-articular arthritis affecting small and large joints, so if you have
more than 10 joints and one of them is small joint then you say yes and go to the next
step; the serology, if the serology is positive then this is definitely RA (serology means
RF OR ACPC).
If serology is negative then you look to the duration; if it is 6 weeks and more then it is
RA. If it is shorter than 6 weeks then you go to APR (Acute Phase Reactant, CRP &
ESR), If the APR positive then it is RA, if it is negative still not diagnosed.
Most of the patient, the APR is positive and the serology: 75% is positive.
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The dr. didnt explain this table and its not for
memorization.
The dr. said that the treatment is very complicated but the main action of drugs is that
they block the inflammatory mediators (TNF, iL 6, 2). And the earlier we diagnose and
the earlier we treat, the higher percentage the person will go to remission.
NAIDs are not good, they dont decrease the progression of the disease & nobody goes
into remission.
Prednisolone by itself dont make a difference (it increase CVS mortality) but if
combined with disease modifying drugs [DMARDs], theres some evidence about
increase the probability of remission.
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Epidemiology:
SLE is the most common connective tissue disease, the risk increases according to:
1) AGE: the peak of the age onset is between 15-40 years old [20-30 in the book] because of
complications as pregnancy, but it can affect any age.
2) SEX: around 90% of affected individuals are females. During the childbearing
age, the ratio is 10:1.
3) RACE: high prevalence in African in US and UK 1:250-500,also in high
prevalence in Latino and Asian.While rare in Africa. Caucasian prevalence
1:2000.
The overall 5 years survival of SLE is 90%. And the mortality within 5 years of
diagnosis occurs due to organ failure or overwhelming sepsis, both of which are
modifiable by early effective intervention.
>> The dr. said that he dont know the prevalence in Jordan and how much the
problem is but this disease is a bad disease, theres no one year without losing few
patients with lupus so its associated with high mortality (young females) and
morbidity.
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Clinical features
1) General Features:
2) Raynaud syndrome
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3) Dermatological features:
4) Gastrointestinal features:
Oral ulcers:
Oral or nasopharyngeal ulceration, usually painless, observed
by physician
and
petechiae.
Also
In old days; 20 years ago, the rheumatology was only an observational specialty, there
was no medications except methotrexate. So they was saying that the difference
between RA & SLE arthritis that SLE is non-erosive (but not 100% !!) with deformities.
Arthralgia: migratory arthralgia with early morning stiffness.
tenosynovitis and small joint synovitis that can mimic RA.
6) Pulmonary features::
Pleuritis: the most common [30%] in life time of SLE patient.
Pneumonitis, pulmonary embolism, pulmonary hypertension, pulmonary
fibrosis & nodules
Pulmonary hemorrhage: the most dreadful with 50 % mortality with treatment.
Usually, males with SLE die because of pulmonary hemorrhage.
< It can cause any disease in the lung >
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7) Cardiovascular features:
Pericarditis: the most common.
Aortic insufficiency: the most common valvular lesion (it damages the valves)
Endocarditis, aortitis, myocarditis, valvulitis and antibiotic prophylaxis
indicated for dental and surgical procedures
Accelerated atherosclerosis & damage to the coronaries (CAD) with 10 times higher
mortality from myocardial infarction from age and sex matched.
Serositis: it includes:
- Pleuritis: convincing history of pleuritic pain, pleural rub heard by a physician or
evidence of pleural effusion, with dyspnea. OR
- Pericarditis: documented by ECG, pericardial rub or evidence of pericardial
effusion.
< So, SLE can affect the pleura or inside the pleura >
8) Hematological features:
Hemolytic anemia with reticulocytosis & mild jaundice & LDH
>> usually, in hemorrhage, if the bone marrow still working, reticulocyte count will
increase but if the bone marrow isnt working (aplastic crisis bcz of lupus),
reticulocyte count will decrease. But in normal person, reticulocyte count will
increase bcz the bone marrow will push more reticulocytes to the blood.
Leukopenia: less than 4,000/mm total on 2 or more occasions OR
Lymphopenia: less than 1,500/mm on 2 or more occasions OR
Thrombocytopenia: less than 100,000/mm, in the absence of offending drugs.
9) Renal features:
Lupus
Impaired kidney function, as if creatinine level increases, then you should treat or
the patient will develop renal failure.
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** Lupus nephritis predict out come (prognosis); the kidneys are the target of lupus, if
the kidney function is normal then the outcome is acceptable -except if theres other
serious organ involvement** Major cause of mortality & morbidity.
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Labs in SLE
>> ANA: 95% positive, sensitive but not specific. 5-10% positive general population,
also positive in other auto immune diseases (eg. thyroiditis)
>> Anti-DNA antibody: specific but not sensitive, increase with active disease. 3060% of patients are positive.
>> Anti-smith antibody: specific for SLE. 30% are positive.
>> Rheumatoid factor: can be positive in 30%.
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This is the most common of the familial periodic fever, predominantly affecting the
Middle East, south Europe.
Autosomal recessive (so you need 2 mutations) disease characterized by attacks of
serositis and fever, attacks are acute and sudden (last from 6-96 hrs; few hours to
days); it come and resolve alone or by NSAID.
First attack occur before age 20 in 90%.
Symptoms: Abdominal pain in 95%, mostly as acute abdomen and peritonitis but
some times mild, Mono-arthritis with effusion in 75%, mostly knees, ankles or
wrists, Chest pain/ pleuritis (unilateral)in 30%, Pericarditis (rare 1%) WITH fever or may be fever alone-.
The main complication of this disease is amyloidosis; any chronic inflammation can
end with amyloidosis as RA. So its a chronic recurrent inflammation that ends with
amyloidosis and the most sensitive organ to amyloidosis is the kidneys so they end up
with dialysis.
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Genetics: the responsible gene has been located in short arm of chromosome 16,
MEFV gene encodes protein (pyrin, marenostrin), Pyrin mostly in cytoplasm of
neutrophils or monocytes /regulates inflammation [regulates neutrophil mediated
inflammation by indirectly suppressing the production of IL-1].
>> mutations: 28 mutation (most common), M694V and V726A.
>> M694V associated with more severe disease and higher risk of amyloidosis
THE END
Best of luck ALL da3watkom :D
Done by: Sara AL-Zu'bi
& Hadeel Al-Kofahi.
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