Here is an essay on ‘Rheumatology’ for class 8, 9, 10, 11 and 12. Find paragraphs, long and short essays on ‘Rheumatology’ especially written for school and medical students.
Essay on Rheumatology
- Essay on the Introduction to Rheumatology
- Essay on the Classification of Rheumatology
- Essay on the Clinical Presentations in Rheumatology
- Essay on the Epidemiology of Rheumatology
- Essay on the Important Guidelines about the Use of NSAID in Rheumatology
Essay # 1. Introduction to Rheumatology:
The Greek word “Rheumatism” means catarrhal changes of the mucus. In large number of joint disorders, there is actual alteration of the joint mucin, the polysaccharide hyaluronic acid. Some like to term this group of diseases as arthritis, i.e. lesions in the articular and periarticular structures. Though difficult, a working definition is suggested.
Rheumatology is the science of rheumatic diseases, affecting articulo-periarticulo-muscular structures (loco-motor system) and other connective tissues of the human body (systemic diseases), characterised by pain, swelling, stiffness and limitation in the joints, with other systemic symptoms and signs.
Essay # 2. Classification of Rheumatology:
There are a large number of rheumatic diseases or arthritis, little over 100 in number, known from ancient times all over the world. In India ‘Ayurvedic system’, all kinds of chronic joint disorders with pain are termed ‘BAT’. The “International League against Rheumatism” and “American Rheumatism Association”, both had presented two different big lists or classification charts.
For practical purposes, we may simplify them into seven major groups:
I. Inflammatory Group of Rheumatic Disease of Known Infectious Agents:
(a) Bacterial Brucella. Gonococcus. Mycobacterium tuberculosis. Pneumococcus. Staphylococcus. Salmonella. Streptobacillus Moniliformis (Haverhill fever). Treponema pallidum (Syphilis). Treponema pertenme (Yaws) etc.
(e) Parasitic etc.
II. Inflammatory Polyarthritis of Unknown Aetiology:
(a) Rheumatoid arthritis. Still’s disease. Psoriatic arthritis. Reiter’s Syndrome
(b) Ankylosing Spondylitis
(c) Rheumatic Fever
(d) Group of “Intermittent Periodic Arthritis Syndromes”
(e) Enteropathic Arthritis.
III. Degenerative Joint Diseases:
(A) Axial or Spinal involvement, e.g. Spondylosis
(B) Peripheral (Proximal/Distal), e.g. Osteoarthrosis (Osteoarthritis)
They may be:
(a) primary, or
IV. Traumatic and/or Neurogenic Disorders:
(a) Traumatic arthropathy, — due to direct trauma resulting in haemorrhage, exudation, and injury to different musculo-skeletal structures (articular & periarticular)
(b) Postural and occupational group — due to indirect trauma, stress or strain, etc.
(c) Neurogenic arthropathy, — charcot’s joint, shoulder-hand syndrome. Syringomyelia, diabetic neuropathy.
V. Arthritis Related to known Metabolic, Biochemical or Endocrinal Disorders of Bones and Joints:
(a) Gout, pseudogout, articular chondro-calcinosis
(b) Onchronosis, hematochromatosis & Wilson’s disease
(c) Rheumatic disorders in endocrinopathies — in hyperparathyroidism, acromegaly,
(d) Haemoglobinopathies (e.g. Sickle cell disease)
(f) Gaucher’s disease
(g) Scurvy (hypo-vitaminosis C).
VI. ‘Connective Tissue’Disorders, including “Diffuse Collagen Diseases”:
(a) Systemic lupus erythematosus. (S. L. E.)
(b) Polyarteritis nodosa
(c) Scleroderma (Progressive systemic sclerosis)
(d) Polymyositis and dermatomyositis
(e) Mixed connective tissue diseases (M.C.T.D.).
VII. Non-Articular Rheumatism or “Painful Syndromes”:
(a) Intervertebral disc lesions, and low back syndromes
(b) Tendinitis, peri-tendinitis, bursitis etc.
(c) Fibrositis, myositis and myalgia, fascitis
(e) Carpal tunnel syndrome
(f) Shoulder-hand syndrome, etc.
Besides, the above seven classical groups, “Tumour and Tumour like conditions”, e.g. multiple myeloma, synovioma, giant cell tumour of tendon sheaths, metastatic lesions in bones & joints, benign tumours of articular tissues present painful joints with rheumatic disorders.
Essay # 3. Clinical Presentations in Rheumatology:
(i) History Taking in Rheumatology:
It is needless to emphasize the importance of skillful history taking in rheumatology, as in all other types of diseases.
Some special questions are to be answered, regarding the joints:
(a) How it started? Sequence of involvement of joints
(b) Number of joints involved, with locations-axial or peripheral, proximal or distal.
(c) Pattern of joint involvement-symmetrical or asymmetrical; migratory, or shifting; or multiple joints involved at a time.
(d) Time-intensity — Acute or chronic; periodical or constant; self-limiting or progressive.
(e) History of trauma is to be noted- direct or indirect; chronic stress & strain; occupational stress or trauma; posture in lying, sitting, standing & working.
(ii) Subjective Symptoms Local & General:
Pain is the chief symptom of the rheumatic disorders, which causes immense suffering, and results in physical and mental disability. This unpleasant sensory manifestation must be thoroughly understood. Its site (from superficial or deep structures), time-intensity, nature (acute, chronic, sharp, dull etc.), character (depending on structures involved), distribution (localised, diffuse, referred etc.) time period (continuous, intermittent etc.) are to be noted and analysed.
Similarly, the results of pain, e.g. crepuscular rigidity, tenderness, mental reaction, and other reflex clinical phenomenon’s are to be correlated. So proper analysis of pain help in the diagnosis and management.
It may be to articular swelling, or of periarticular origin. Morning stiffness, stiffness after rest, transitory, periarticular swelling of O.A. etc. Muscle guard or spasm resulting from pain, may give rise to stiffness. So magnitude, particular time, duration and accompanying features with stiffness are to be recorded.
(c) Limitation of Movements:
Limitation of movements in the joints — may be due to pain, internal joint structure involvement, or ankylosis. Periarticular structures and muscle spasm or contractures may cause limitation. The amount in degrees and range of limitation, i.e. inner, middle or outer range should be mentioned.
Swellings are of different natures — fluctuating or tense swelling may be due to effusion or exudation inside the joints; hard swelling due to bony overgrowths; firm periarticular soft tissue swelling etc.
(e) There may be other systemic symptoms, e.g. atrophy, fatigue, emotional disturbances, etc.
(iii) Objective Signs and Methods of Examination:
e.g. swelling, tenderness, local sign of inflammation etc, are to be detected by clinical examination as stated below:
A. Local Examinations are made, and a joint chart is maintained.
I. Inspection (Look & Compare):
(a) Skin — Colour changes, shiny or tense, abnormal creases, any break etc.
(b) Contour or shape of joints and limbs, swelling, wasting, shortening etc.
(c) Position and alignment — of joints and limbs.
(d) Any deformity or not.
II. Palpation (Feel & Compare):
It is moist or dry, rough or smooth, warm or cold, skin sensations — are charted graphically.
(b) Soft Tissues & Joints:
1. Swelling as discussed.
2. Tenderness — localised, or “all over”; gradation of tenderness:
Grade I. — Patient complains of tenderness on deep pressure.
Grade II. — Patient whines on deep pressure.
Grade III. — Patient ‘withdraws the part’ on localised pressure.
Grade IV. — Patient withdraws before the part is touched — ‘touch me not’ attitude, tenderness all over due to inflammation, e.g. gout, and acute inflammatory flares.
3. Thickened synovium, or other structures, can be felt.
4. In case of any soft tissue swelling — its shape, size, surface, consistency, edge and attachments should be determined.
5. Fluid accumulation in the joints should be determined by ‘fluctuation test’, ‘tap method’ and ‘bulge test’, by demonstrating the displacements of fluid.
6. Joint stiffness, or laxity (subluxation and dislocation) are recorded.
7. Crepitations – are different natures, – e.g. coarse bony grating, coarse cartilagenous crepitations, medium cartilagenous crepitations and rubbing, fine soft tissue crepitation and rubbing.
8. Signs of inflammations- Heat, erythema, etc.
Bones are to be palpated for tenderness, localised thickening, shortening, any irregularity of surfaces, any bony growth, or spurs, or nodes, or lumps. The size (progressively increasing or not?), shape, site, edge, consistency and tenderness of any abnormal bony lump should be determined. Any bending of the-bones is to be noted.
III. Movements in Joints (Move and Compare):
(a) Active movements through full range, and any limitations and pain in particular ranges are noted. .
(b) Passive movements through permitted full range are performed to find out any limitation and pain in any range; any increased or abnormal movements.
B. General examination of the different systems of the body.
Skiagram and laboratory tests are definitely of much help, which will be also discussed with individual diseases.
IV. Joint Deformity:
Whether postural or structural (fixed), congenital or acquired is to be determined.
V. Muscle Power:
Muscle Power is tested and noted numerically – 0,1,2,3,4 & 5; and a progress chart is maintained. Any wasting deficiencies is noted.
VI. Functional Testing:
Functional testing should be done at intervals and ‘Activities of Daily Living (A.D.L.) chart and ‘Work Chart’ are to be maintained.
VII. Some special clinical tests for different regions (Specific Rheumatological Examinations) are done to help in the diagnosis of different diseases, which will be discussed with different diseases.
Special X-Ray Examinations:
1. Joint Structures Examinations:
Synovial Fluid Analysis:
Synovial fluid analysis may be done after it is aspirated aseptically, in the following ways:
A. General Examination:
1. Volume — normal, increased, or diminished.
2. Colour — clear to pale yellow (normal), white, purulent, or xanthochromic (yellow) Blood fluid is due to trauma.
3. Clarity — transparent (normal), opaque, or translucent.
4. Viscosity — normally very high; may be low or very low (watery).
5. Mucin clot — good (normal); fair, or poor.
6. Spontaneous Clot — Normal synovial fluid does not clot, as it lacks in fibrinogen, prothrombin, factors V and VII etc. But pathologic fluids do clot; rapidity and size vary with the underlying lesion.
B. Microscopic Cytology:
1. Total W.B.C. count per c.m.m.
Normal = less than 150. Increased in pathological conditions. In degenerative lesions up ‘to 3,000 and in inflammatory conditions 3,000 and much above.
2. Differential Leucocytic Count:
Normal — polymorphonuclear cells are less than 25%. In inflammatory lesions — much above 25%, up to 90% even.
3. Wet Smear Inspection by Polarised and Phase Contrast Microscopy:
(a) “Inclusion body cells” or “ragocytes” (rasin cells), originally called “RA Cells”. It is not disease specific, may be found in joint fluids of inflammatory disorders. They are polymorphonuclear leucocytes with ingested or phagocytosed material, including immunoglobulin G and M.Rh factors, fibrin, antinuclear factors, immune complexes and DNA particulars.
(b) Classic “L.E. Cells” are seen in Write’s stained smears. It consists of a W.B.C. with a large purple-red homogeneous globulin inclusion body, which compresses the nucleus against the cell membrane.
It must be differentiated from “tart” cells, polymorphonuclear W.B.C. that have phagocytosed nuclear debris.
(c) “Reiter’s Cells” are not again disease specific (an inconstant feature of Reiter’s syndrome) has been found in many inflammatory joint fluids. The cells are macrophages with ingested polymorphs (dead and degranulated).
(d) In rheumatoid arthritis, the synovial fluid is found to contain a large number of lymphoblasts, over half of all large mononuclear cells.
C. Microbiologic Tests:
(a) Culture for bacteria, fungi, viruses, or tubercular bacilli.
(b) Smear & culture of joint fluid for microbes, for detection of their antigens by counter- current immuno-electrophoresis.
D. Serologic Tests:
(a) Total protein content – Normal – 1.8g/dl.
(b) Total Haemolytic Complement (C H50) — Titration- It measures the functional activity pf all complement component proteins in synovial fluid — Normal — very low level of C’ H50.
E. Chemical tests for:
II. Synovial membrane — Biopsy & histology
III. Subchondral Bone
IV. Articular Cartilage
Extra Articular Biopsy:
(i) Subcutaneous Nodules and other depositions.
(ii) Muscle Biopsy.
To determine the type of anaemia, Mean Corpuscular Volume (MCV) and Mean Corpuscular Haemoglobin (MCH), should be determined:
The study of lymphocytes and lymphoblasts are important. Inclusion bodies and abnormal cells were discussed under Synovial fluid examination.
Erythrocyte Sedimentation Rate (ESR):
It is the “single important laboratory test” which indicates and is proportionate to the inflammatory activity in the connective tissue diseases. It is the property of the plasma component, and is influenced by the fibrinogen, and alpha-and gamma-globulins content in plasma.
It is not a specific or diagnostic test, ESR is normal in degenerative conditions and fibrositis. In congestive heart failure, especially in young patients with rheumatic carditis, the E.S.R. is lowered. According to some rheumatologists, the C-reactive protein (CRP) and hepatoglobin are more accurate than the ESR for serial evaluation of rheumatoid activity and are not depressed by hormone therapy.
The invading agents (e.g. bacteria, rickettsia, virus etc.) and foreign antigens trigger on the defensive mechanism (immunocomplex response) of the body to produce antibodies (which are of different types and natures) and ‘antigen-antibody complexes’.
Immunoglobulin (Ig) are antibodies and are heterogenous proteins, synthesised primarily in plasma cells, and is formed in serum and extra-cellularfluids.
Five major classes of immunoglobulin; (Ig) are:
IgG, IgA, IgM, IgD, and IgE.
They are studied by electrophoretic and immuno electrophoretic analysis of serum and urine.
‘Antigen – antibody complexes’ again activates the compliment system consisting of 18 plasma proteins, which helps the defensive mechanism of the host to recognise the foreign antigen and to generate the mediators. They are responsible for haemolysis of antibody sensitised B.B.C.
Sometimes, the defensive reactions become “out of bounds” and produce antibodies against host’s own structures, without recognising them. They are called ‘auto-antibodies’, e.g. antinuclear antibodies (ANA), anti-DNAantibodies etc. They are useful in diagnosis and prognosis of the cases.
Essay # 4. Epidemiology of Rheumatology:
A disease should be understood and studied from all aspects, so that it can be efficiently diagnosed, treated and controlled. Epidemiology means the effect of the disease on population at large. (‘Epi’ means upon; ‘demos’ means people; ‘logy’ means science).
The methodology includes the study of prevalence, distribution, and all the associated factors related to the disease, by population survey.
The following aspects of the disease are recorded and studied:
1. Prevalence (P), incidence or rate of occurrence (I), average duration of the diseases (D), in a given population, of a demarcated area. P = I X D. are determined.
2. The following factors which influences the disease incidence (I) and prognosis are- ‘Onset- age’, Sex, Races and Socio-economic condition, etc.
3. The disease is studied and ‘classified’; and also specified with ‘Diagnostic Criteria’ determined.
4. Sensitivity and specificity of the disease in a given population.
5. Where the disease is infectious or communicable or not.
6. The methods of control of the disease.
7. The ‘causation’ of the disease, and the associated factors, i.e. the complete aetiology is thoroughly studied.
In rheumatology, most of the disease have multifactorial aetiology; interactions of those factors with the body’s defensive mechanism produces a complicated immuno-complex. pathogenesis. These interactions of multiple factors are related to the ‘Host’, ‘Causative agents’ and ‘Environmental conditions’. Primary cause of aetiology is thus obscured, and the triggering factors come to the limelight, which are either exogenous precipitating factors, or endogenous predisposing factors in the host.
Epidemiological studies show a large number of factors influencing the disease, but the original definite cause or infection is still not known. The initial primary infection of short duration starts an immuno-complex mechanism in the body, which again sets up secondary infection or infection-like mechanism affecting some selected structures (e.g. joints) along with systemic manifestations giving rise to the characteristic picture of the disease.
The ‘Host factors’ influencing the disease are Age, Sex, Race, Hereditary factors, different susceptible systems or organs of the body, etc. The causative agents may be bacteria, virus, mycoplasma, or rickettsia with their antigenic structures. The environmental conditions influencing the disease are toxic materials, climatic conditions, geographical distributions etc.
The aim of this article is to impress the importance of studying the rheumatological disorder from different scientific angles to diagnose them specifically, and to treat and rehabilitate the chronically ill patients in the society as tolerant, productive and happy individuals. The incidences of these diseases are no more thought to be rare in this country as in the past.
With the increased expectation of life, increased stress and strain of modern life, and better diagnostic methodology are bringing more rheumatological cases to the limelight, not only in this country but all over the world. The medical students and the clinicians are expected to get more benefit from reading this article, once before and re-reading it again after they have studied the individual diseases.
To conclude, a simple survey-chart of some of the rheumatological disorders or syndromes are presented to have a glimpse of the diseases to be studied.
Essay # 5. Important Guidelines about the Use of NSAID in Rheumatology:
(1) Many new drugs have appeared in the market in recent years and it is becoming difficult choose a safe drug as almost of all of them are capable of producing gastrointestinal complications liver damage, blood dyscrasias, renal failure, toxic epidermal neurolysis and Stevens Johnson syndrome (Brit. Med. Jour. Vol.292, 1986 CMS update pages 1190-1191 gives an excellent details of drug reaction due to NSAID).
(2) It is advisable not to prescribe these drugs wherever possible and avoid it in cases of peptic ulcers or of there is history of P.V. disease.
(3) Always it should be given after meals and antacids.
(4) Start with minimum dose and in Editor’s view salicylates, aspirin (being cheapest and effective) and Ibuprofen are best drugs to start initially.
(5) Avoid use of indomethacin indiscriminately specially slow-release indomethacin preparations are dangerous.
(6) Sale of these drugs over the counter without prescription should be stopped.
(7) Combination of NSAID with oral steroids may also be done after very careful consideration.
(8) Watch for adverse drug reactions.
(9) Assess hepatorenal health while prescribing these drugs.
(10) Regular follow-up is essential.