GOD Cant Come in Person to Help You.

He Will Send Some One in the

Form of Homosepian, Believe it. The Only Thing What You Are Going to
Take Away is Karma _Educate_Dr P Kumar, BIO-GEN.

COGNITIVE CONCEPT MAP ON AUTOIMMUNE DISORDERS THAT AFFECTS MSK SYSTEM

Problem Based Learning (PBL)_Large Groups Medical Students: e-Problem Solving Test: Rheumatoid Arthritis & Gout Syndrome (GS)
*International Medical University (IMU),
ST Matthews School of Medicine (SMU),
AIMST-U, MSU, Vinayaka Missions Med School
International Medical School (IMS, MSU)

Dr Kumar Ponnusamy , Dr Jegathambigai RN & Dr Senthilkumar Rajasekaran*

*
1
International Medical School (IMS), Management & Science University (MSU), AMU,Malaysia
*

Acknowledgements: The Authors Gratefully Acknowlwdges All On-Line Resources Including Google.com, PubMed, Elsieviers Ltd, Lippincotts, Haplan.Com, Scribd.com., ect.,.

RHEUMATOID Arthritis (RA): Autoimmune Disorders That Affect the Musculoskeletal System:

RA. Chronic, systemic autoimmune disease. Inflammation of connective tissue in diarthrodial (synovial) joints, Periods of
remission and exacerbation, Frequently accompanied by extra-articular manifestations. Occurs globally, affecting all ethnic groups. Occurs at any time of life, Incidence increases with age, Peaks between 30s and 50s. Nearly 2.1
million Americans affected. Women have incidences three times higher than men. Etiology: Two etiologies: Autoimmune etiology-Most widely accepted. Genetic factor etiology. Etiology and Pathophysiology: RA progresses in four
stages (cont'd). Stage 3: Severe-X-ray evidence of cartilage and bone destruction in addition to osteoporosis; joint deformity; extensive muscle atrophy; possible presence of extra-articular soft tissue lesions. Stage 4: TerminalFibrous or bony ankylosis, stage III criteria. Clinical Manifestations Joints-Specific articular involvement, Symptoms occur symmetrically, Frequently affect small joints of hands and feet, Larger peripheral joints may also be
involved. Clinical Manifestations- Joints-Patient experiences joint stiffness after periods of __. Morning stiffness may last from 60 minutes to several hours or more, MCP and PIP joints typically swollen. Fingers may become
spindle shaped from synovial hypertrophy and thickening of joint capsule. Joints become tender, painful, and warm. Joint pain: Increases with __ , Varies in intensity, May not be proportional to degree of inflammation,
Tenosynovitis frequently affects extensor and flexor tendons near wrists , RA progresses. Extra-articular Manifestations: Three most common; Rheumatoid nodules develop in up to 25% of all patients with RA, Those affected
usually have high RF titers. Clinical Manifestations-Extraarticular Manifestations: Sjgrens Syndrome, Seen in 10% to 15% of patients with RA Can occur as a disease by itself or in conjunction with other arthritic disorders RA
and systemic lupus erythematosus (SLE). Complaints of burning, gritty, itchy eyes, Decreased tearing, photosensitivity . Feltys syndrome: Most commonly in patients with severe, nodule-forming RA, Characterized by
Inflammatory eye disorder, Splenomegaly, Lymphadenopathy, Pulmonary disease, Blood dyscrasias . Complications: Joint destruction begins as early as first year of disease without treatment, Flexion contractures and hand
deformities , Cause diminished grasp strength . Affect patients ability to perform, self-care tasks, Cataract development and loss of vision can result from scleral nodules. Rheumatoid nodules: On the skin can ulcerate, similar to
pressure ulcers, On vocal cords leads to progressive hoarseness, In vertebral bodies can cause bone destruction. Cardiopulmonary effects may occur later in RA, pleurisy, pleural effusion, pericarditis, pericardial effusion,
cardiomyopathy, Carpal tunnel syndrome can result from swelling of synovial membrane. Diagnostic Studies: RA is defined as having at least 4 of the following seven criteria. Following must be present for at least 6 wks: Morning
stiffness that lasts 1 hour, Swelling in three or more joints, Swelling in hand joints, Symmetrical joint swelling, Erosions or decalcification seen on hand x-rays, Rheumatoid nodules, Presence of serum RF. Diagnostic Testing:
History & PE: Blood Studies: Rheumatoid factor (RF), Erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), Antinuclear antibodies (ANA) titers are seen in some. Synovial fluid analysis: Straw-colored fluid with
fibrin flecks. WBC is elevated to >25,000/l. X-rays: Will not confirm diagnosis-only show bone changes. Collaborative Care: Care begins with a comprehensive program of education and drug therapy Education of drug therapy,
Patient and family educated about disease process and home management strategies Involve PT and OT. Drug Terapy: Drugs remain cornerstone of treatment DMARDs can lessen permanent effects of RA. Choice of drug is based
on patients: disease activity, level of function, lifestyle considerations: e.g; choices for a woman of childbearing age? . Treatment and Nursing Care for Rheumatoid Arthritis: See Table 65-3 for meds used for arthritis p. 16981700: Salicylates, NSAIDs, Antibiotics, Topical. .
analgesics, Corticosteroids, DMARDs, Gold compounds, Antimalarials, Immunosupressants, Biologic/Targeted therapy. Methotrexate (Rheumatrex) is drug of choice, Rapid antiinflammatory effect decreases clinical symptoms
in days to weeks Inexpensive Lower toxicity compared to other drugs Side effects: bone marrow suppression, hepatotoxicity. Other DMARDs for mild to moderate disease Sulfasalazine (Azulfidine), Antimalarial drug
ydroxychloroquine, Leflunomide (Arava) - a newer synthetic: DMARD that blocks immune cell overproduction . DRUG THERAPY: Biologic/targeted drug therapies can also slow disease progression in RA. Can be used in
patients with moderate to severe disease who have not responded to DMARDs or in combination therapy with an established DMARD. Corticosteroid therapy can aid in symptom control Intra-articular injections may relieve pain
and inflammation associated with flare-ups. Long-term use should not be a mainstay, Risk osteoporosis, avascular necrosis. Low-dose prednisone for a limited time to decrease disease activity until DMARD effect is seen. Various
NSAIDs and salicylates are used to treat pain and inflammation Aspirin is often used in high dosages of 4 to 6 g/day (10 to 18 tablets), NSAIDs have antiinflammatory, analgesic, and antipyretic properties; f ull effectiveness may
take 2 to 3 weeks. Combination Drug Therapy: Use of two more drugs simultaneously, Can slow symptoms and joint damage while improving function , Often include a DMARD, an NSAID, and a corticosteroid . Revlieve Pain:
NSAIDs, DMARDs Non-Pharmacological, Heat or Cold applications, Rest, Relaxation techniques. Nursing Manaement Intervensions, Nonpharmacologic relief of pain . Therapeutic heat and cold, Rest, Relaxation techniques,
Joint protection, Biofeedback Transcutaneous electrical stimulation , Hypnosis. Heat & Cold Therapy: Help relieve pain, stiffness, and muscle spasm, Ice, Superficial heat sources. Psychological Support: Patients value system and
perception of disease must be considered. Patient is constantly challenged by problems of: Limited function and fatigue, Loss of self-esteem, Altered body image, Fear of disability or deformity.
Moist heat, Superficial heat sources, Moist heat, Ice, Superficial heat sources, Moist heat. NSAIDS may be used when patient cannot tolerate high doses of aspirin .

GOUT: Deposits of sodium urate crystals in articular, periarticular, and subcutaneous tissues. May be primary or secondary. -

Other Crystal Arthropathies

BIOCHEMISTRY

Ack: KAPLAN.COM

hereditary error of purine metabolism. Secondary-drugs that inhibit uric acid excretion or increase rate of cell death or another
acquired disorder. Incidence and Risk Factors: Primary gout accounts for 90% of cases. Affects primarily middle aged men, Risk
factors: obesity, HTN, thiazide diuretics, excess alcohol use. Pathophysiology: Uric acid is end product of purine metabolism and
is excreted by the kidneys, Causes of hyperuricemia, Diet high in purines will not cause gout, but may trigger an attack in a
susceptible person. Clinical Manifestations of GA: Gouty arthritis in one or more joints (but less than four), Great toe joint most
common first manifestation; other joints may be the foot, ankle, knee, or wrist. Joints are tender & cyanotic, May be precipitated
by trauma, surgery,, alcohol ingestion, or infection. Onset usually nocturnal, with sudden swelling and excruciating pain, May
have low grade fever, Usually subsides within 2-10 days, Joints are normal, with no symptoms between attacks.
Complications: Joint deformity, Osteoarthritis, Tophi may produce draining sinuses that may become infected, Renal stones,
pyelonephritis, obstructive renal disease. Diagnostic Studies : Serum uric acid levels May be caused by other factors. WBC
elevated during acute attack, ESR 24 hour urine uric acid levels. Synovial fluid aspiration contains uric acid crystals, Seldom
necessary. X-rays appear normal in early stages; tophi appear as eroded areas of bone. Collaborative Care: Acute
attack: Colchicine produces dramatic antiiflammatory effects with relief within 24-48 hours, NSAIDs for additional pain relief.
(Anturane) inhibit tubular reabsorption of uric acid. febuxostat (Uloric) inhibits xanthine oxidase, recently shown to reduce
serum uric acid levels. Uricosuric Agents: Probenecid (Benemid): Precautions. Sulfinprazone (anturan) block resorption uric acid,
High fluid intake, alkaline urine. Not effective if creatinine clearance is elevated. Cozaar: Angiotension II receptor angonist,
Monitoring, Force Fluids while on these medications!. Dietary measures: Weight reduction: Avoidance of E-OH. Avoidance of
foods high in purines: High: Sardines, anchovies, herring, mussels, liver, kidney, goose, venison, meat soups, sweetbreads, beer &
wine. Moderate: Chicken,, salmon, crab, veal, mutton, bacon, pork, beef, ham.. Treatment & Nursing Care: Bed rest and position
for comfort. Joint immobilization and protect joint from pressure. Local application of heat or cold. Assess for complications:
Formation of kidney stones Hypertriglyceridemia, Hypertension. Prevention of renal stones: Increase fluid intake to maintain
adequate urine output. Allopurinol, ACE inhibitor losartin (Cozaar)-promotes urate diuresis.

PATHO-PHYSIOLOGY

Purine_Uric Acid Metabolism

Microscopic View Demonstrates the
Needle Shaped Uric Acid Crystals

Diagnosis of Gout: Synovial Fluid Analysis:

CPPD crystals might not be as evident as MSU crystals.
Detection might not be as accurate if fluid analysis is
delayed. In addition, because pseudogout and gout can
coexist, MSU crystals might also be observed. Radiographs:
Chondrocalcinosis in the joint involved and other more typical
joints even if pseudogout is not clinically active at the time of
presentation. They are not required to make the diagnosis once
CPPD crystals are seen under polarized light.

Research Component on RA

Review Article on RA
Note & Disclaimer: The content in this e-Cognitive Concept Map on
BIO-GEN is based on the knowledge that I acquired studying regular
reference books and On-Line Learning Resources in Google, PUBMed
ect., and after years of teaching biochemistry-Genetics to Medical and
Allied Health Science students in PBL Based Integrated Med Curriculum.
The sourvce of the figures, animation used in this Map is mentioned
where ever applicable, and they are used purely for teaching
Biochemistry-Genetics to audience and no monetary benefit intended out
of it. If copyright owner of the figures used in this Map do not agree with
this disclaimer, they are welcome to contact me about it and, I will delete
their content and source from my presentation. Thanking You!.

Treatment
Acute: If one or two joints: joint aspiration and IA steroid injection. If more than
two joints are involved treatment is directed more toward systemic
therapy (NSAIDs, corticosteroids, colchicine). Chronic: In patients
with three or more attacks a year colchicine at a dose of 0.6 mg once
or twice daily to reduce the number of attacks in a year. There are no
hypouricemic equivalents to improve the long-term control of pseudogout and to prevent or reverse CPPD crystal deposit disease.

PLEOTROPY

References: [1] [1]. Iain B. McInnes and Georg Schett. Mechanisms of Disease The Pathogenesis of Rheumatoid Arthritis. N Engl J Med
2011;365:2205-19. [2]. Hyon K. Choi, David B. Mount and Anthony M. Reginato. Pathogenesis of Gout. Physiology in Medicine: A series
of articles linking medicine with science. Ann Intern Med. 2005;143:499-516.
[3]. Google.com, Entrez PUBMed.Com, Scienceditect.Com.
[4] . Lippincotts Biochemistry.