submitted by :- m abdelmotaal department of pharmacology 1
TRANSCRIPT
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Submitted By :- M Abdelmotaal
Department of pharmacology
Rheumatoid arthritis & Gout
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(RA) is an autoimmune disease that causes chronic inflammation of the joints & can also cause inflammation of the tissue around the joints .
Inflammatory arthritis
Peak incidence in 3rd to 4th decades(عقود ) of life
3-5 times higher preponderance(( يكثر in females than males
Rheumatoid Arthritis
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Exact(الدقيقة) mechanism is not known 1) Autoantibody-Rheumatoid factor(R.F.) : R.f. is Anti-IgG
2)other autoantibodies:Antinuclear factor(ANF)Antibodies to Collagen type-2 classAntibodies to cytoskeleton
Etiopathogenesis
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3) Activation of cell-mediated immunity which is observed by numerous inflammatory cells
4)Trigger events :- Local/systemic infection It includes some infectius agents such as Epstein-Barr Virus(EBV) cytomegalovirus(CMV) rubella
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Longitudinal Course of RA
Reproduced with permission from McInnes IB, et al. Nat Rev Immunol. 2007;7(6):429-442.
CCP, cyclic citrullinated peptide; CTLA4, cytotoxic T-lymphocyte antigen 4; GP39, cartilage glycoprotein 39; PADI4, peptidyl arginine deiminase, type IV; PTPN22, protein tyrosine phosphatase, non-receptor type 22.
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Rheumatoid Arthritis
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Tender , warm , swollen joints
Joints inflammation often affect wrist & finger joints
Also affect other joints including neck ,shoulder ,elbow ,hips ,knees ,ankles ,feet
Fatigue ,occasional fever ,sense of not feeling well
Pain & stiffness after morning wake up or after a long rest
Signs & symptoms
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By imaging: X-ray MRI Ultra sound
By Blood tests:a)Inflammatory markers:
ESR(erythrocytes sedimentation rate) C reactive protein(CRP) ANA(anti-nuclear antibody)
b)Rheumatoid factor:c)Anti-ccp antibodies : it in 99% gives +ve resultd)Anti-MCV assay(anti-Mutated citrullinated Vimentin)
Diagnosis
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There is no cure for RA,there is some treatments which can modify the disease process.
GOAL for Treatments :1. Relieve pain2. Reduce inflammation 3. slow down or stop joint damage
TREATMENTS
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1)medication2)surgery3)lifestyle
1)medication: Classification:
1. Anti-inflammatory-analgesic drugs2. Anti-inflammatory drugs without direct analgesic action3. Disease Modifying Antirheumatic Drugs(DMRDs)4. immunosuppressants5. TNF-alpha blockers6. Interleukin-1 blockers
Current treatment approaches
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ANTIINFLAMMATORY-ANALGESIC DRUGSEg.aspirin,indomethacin,ibuprofen,naproxen, piroxicam,nabumetone,diclofenac,celecoxib M.O.A:It inhibit pg,& chemicals that are responsible for pain and swelling
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Ibuprofen-: Individuals should not use ibuprofen for more than 10 days for the treatment of pain or more than 3 days for the treatment of a fever unless directed by a physician
Celecoxib: The lowest effective dose should be used for each patient
GLUCOCORTICOIDS-:They are used when disease Is not responding NSAIDs. Have serious side effect incase of high doses Eg.prednisolone:-
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Eg. Methotrexate Hydroxychloroquine Sulfasalazine Gold salts
Remission inducing drugsDMARDs(metho,antiinf,3s sulf,ster,salts
gold)
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METHOTREXATE: It is antimetabolite drug
M.O.A:- It inhibit dihydro folate Reductase enzyme.
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It is antimalerial drug.OH-chloroquine
Sulfasalazine is used to treat rheumatoid arthritis in combination with anti- inflammatory medications. Sulfasalazine is generally well tolerated.
sulfasalazine
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Eg. Gold thioglucose(SOLGANAL) Gold thiomalate (MYOCHRYSINE) Auranofin (RIDAURA)
Gold salts
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Joint replacement
Hip replacement Knee replacement
SYNOVECTOMY
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It is metabolic disorder characterized by hyperuricaemia
Normal plasma=1-5 mg/dl
Stages of gout:-1. asymptomatic hyperuricaemia2. acute gouty arthritis3. intercritical period4. chronic tophaceous stage
GOUT
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Types :- 1)metabolic-10% cases Over production of uric acid
2)renal- 90% cases Reduced renal excretion of uric acid
Causes:- 1)genetic(absence of hypoxanthine) 2)medication:- 3)lifestyle
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Drugs that causes hyperuricaemia : Alcohol Thiazide Cytotoxic drugs Amiloride Isoretinoin Ethambutol Cyclophosphamide
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Acute attack: Over hours frequently nocturnal Excruciating pain Swelling, redness and tenderness Podagra May effect knees, wrist, elbow, and rarely SI and hips
Chronic: Destructive tophacous Much greater chance if untreated nodules
Sign & symptoms
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DIAGNOSIS:-1. X-ray2. Synovial fluid test:-3. Blood test:-
Normal level:1-5mg/dl Above 7 in males Above 6 in females indicate hyperuricaemia. W.B.C.,ESR is increased in gout without infection.
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Uric acid is end product of purine metabolism Monosodium urate has low water solubility When conc. Of MSU is above 7mg/dl,their solubility is
decreased due to saturation and it form crystal.
Pathogenesis
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Goal of treatment:- Relieve pain Reduce inflammation Terminate acute attack Prevent recurrent attack Prevent complications associated with chronic
deposition of urate crysals in tissues.
Treatment
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Classification of drugs no cure alone) 1)NSAIDs 2)colchicine 3)corticosteroids 4)uricosuric drugs 5)xanthine oxidase inhibitor
NSAIDs:- Indomethacin Naproxen Piroxicam diclofenac
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COLCHICINE:- It is an alkaloid from
colchicum autumnale. It is antimitotic drug.
MOA- it inhibit release of
Glycoprotein & subsequent Events.
It inhibit granulocyte Migration into inflamed joints.
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CORTICOSTEROIDS:- Eg.prednisolone They are rarely used.they are used in case of patient which is
contraindicate to NSAIDs. they produce rapid response like colchicine.but it is
contraindicated to patients with renal failure.
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PROBENECID:- It is uricosuric drug. MOA- It is act by inhibiting reabsorption of uric acid.so,excretion
of uric acid is increased.
XANTHIN OXIDASE INHIBITOR:- Eg.allopurinol. It is hypoxanthine analogue. MOA:- It is act by inhibiting Xanthine oxidase which is required for
synthesis of uric acid.
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OA is a group of diseases and mechanical abnormalities entailing degradation of joints, including articular cartilage and the subchondral bone next to it
OA is derived from the Greek word ‘ostoe’, meaning ‘of the bone’, ‘arthro’, meaning ‘joint’, and ‘itis’, meaning inflammation
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Osteoarthritis is the most common type of arthritis. The prevalence increases with age 80% of people over 60 years will have some radiological
evidence of it, although only 60% of those will show symptoms.
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OsteoarthritisEtiology & Pathophysiology
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Osteoarthritis-Xray
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OsteoarthritisX-ray changes
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Osteoarthritis Causes
Primary Osteoarthritis Most CommonThought to be result of AgingDecreased ability to withstand stressLigaments supporting joints weaken
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Secondary Osteoarthritis
Obesity Trauma Surgery
Abnormal joints Gout Diabetes
Hormone disorders
Causes
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Goals of Treatment
To Relieve painIncrease motionImprove strength
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Osteoporosis means "porous bones," causes bones to become weak and brittle – so brittle that even mild stresses like bending over, lifting a vacuum cleaner or coughing can cause a fracture.
In most cases, bones weaken when low levels of calcium, phosphorus and other minerals in the bones and results as low bone density.
A common result of osteoporosis is fractures of the spine, hip or wrist.
Although it's often thought of as a women's disease, osteoporosis also affects many men.
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SYMPTOMS
Back pain, which can be severe if fractured or collapsed vertebra
Loss of height over time, with an accompanying stooped posture
Fracture of the vertebrae, wrists, hips or other bones
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Normal bone has the appearance of a honeycomb matrix (left). Under a microscope,
osteoporotic bone (right) looks more porous.
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CAUSES
The strength of the bones depends on their size and density; bone density depends in part on the amount of calcium, phosphorus and other minerals bones contain.
When the bones contain fewer minerals than normal, they're less strong and eventually lose their internal supporting structure.
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The process of bone remodeling
Scientists have yet to learn all the reasons why this occurs, but the process involves how bone is made. Bone is continuously changing — new bone is made and old bone is broken down — a process called remodeling, or bone turnover.
A full cycle of bone remodeling takes about 2-3 months.
In young – the body makes new bone faster than it breaks down old bone, and the bone mass increases.
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Reaches the peak bone mass in mid-30s. After that, bone remodeling continues, but
loses slightly more than gain. At menopause, when estrogen levels drop,
bone loss increases dramatically. Many factors contribute to bone loss, the
leading cause in women is decreased estrogen production during menopause.
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Risk of developing osteoporosis depends on how much bone mass attained between ages 25 and 35 (peak bone mass) and how rapidly loses it later. The higher peak bone mass, the more bones "in the bank" and less likely to develop osteoporosis as ages.
Not getting enough vitamin D and calcium in the diet may lead to a lower peak bone mass and accelerated bone loss later.
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What keeps bones healthy
Regular exercise Adequate amounts of calcium Adequate amounts of vitamin D, which is
very essential for absorbing calcium
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RISK FACTORS
Sex – Fractures from osteoporosis are about twice more in women than in men. Risk in women at menopause (45 yrs) that accelerates bone loss. Risk in men is greater than age 75.
Age. The older, the higher risk of osteoporosis. Bones become weaker as ages.
Race. Greatest risk – white or of Southeast Asian descent. Black and Hispanic men and women have a lower, but still significant, risk.
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Family history. Frame size. Men and women who are
exceptionally thin or have small body frames tend to have higher risk because they may have less bone mass to draw from as they age.
Lifetime exposure to estrogen. The greater a woman's lifetime exposure to estrogen, the lower her risk of osteoporosis.
Excess soda consumption. Chronic alcoholism. Depression.
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Eating disorders. Women and men with anorexia nervosa or bulimia are at higher risk of lower bone density in their lower backs and hips.
Corticosteroid medications. Long-term use like prednisone, cortisone, prednisolone and dexamethasone, is damaging to bone.
Thyroid hormone. Too much thyroid hormone can cause bone loss.
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Other medications. Long-term use of the blood-thinning medication heparin, the cancer treatment drug methotrexate, some anti-seizure medications, diuretics and aluminum-containing antacids also can cause bone loss.
Breast cancer. Postmenopausal women who have had breast cancer are at increased risk of osteoporosis, especially if they were treated with chemotherapy or aromatase inhibitors such as anastrozole and letrozole, which suppress estrogen.
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Low calcium intake. A lifelong lack of calcium plays a major role in the development of osteoporosis.
Medical conditions and procedures that decrease calcium absorption. Stomach surgery (gastrectomy) can affect the body's ability to absorb calcium.
Sedentary lifestyle. Bone health begins in childhood. Children who are physically active and consume adequate amounts of calcium-containing foods have the greatest bone density. Exercise throughout life is important, but can increase bone density at any age.
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TREATMENTS AND DRUGS Hormone therapy (HT) Prescription medications – Bisphosphonates,
Raloxifene (Evista) / selective estrogen receptor modulators (SERMs), Calcitonin, Teriparatide (Forteo), Tamoxifen.
Emerging therapies – New physical therapy program combines the use of a device called a spinal weighted kypho-orthosis (WKO), a harness with a light weight attached and specific back extension exercises. The WKO is worn daily for 30 minutes in the morning and afternoon.
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ESTROGEN AND BONE PROTECTION
Estrogen is essential for healthy bone, and that when the production of estrogen is reduced,
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PREVENTION
Do exercise. Add soy in diet. Avoid smoking Avoid excessive alcohol. Avoid caffeine, which is very harmful. Consider hormone therapy. Maintain good posture – Prevent falls. Manage pain. Don't ignore chronic pain.
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