Conceptual review of Amavat as per classical approach.

1. Conceptual Study Of
Amavata(Disease review)
Presenter-Vd Bhavisha Sheladiya
M.D. 3rd year Scholar
Dept. of Panchakarma

2. • Guided by :
Vd. Ram Shukla
Assistant Professor
Govt. Akhandanand Ayurveda College,
Bhadra, Ahmedabad.

3. RHEUMATOID ARTHRITIS
DEFINATION:
• R.A is a symmetrical destructive and deforming Polyarthritis
affecting small and large synovial joints with associated
systemic Disturbance, a variety of extra articular features like
Pain, oedema, Carditis, Lymphadenopathy etc. there is a
presence of circulating globuline antibodies in the blood viz. RA
factor.1 (Davidson 1998).

4. EPIDEMIOLOGY:

5. 1.ETIOLOGY:
The exact cause is still unknown. The possible causative factors are:
 Age: Onset of this disease is more frequent in 3rd to 6th decade of life, but less
common before puberty.
 Sex: Females are more prone than males.
 Genetic susceptibility: Although influence of heredity is not known, but still
familial aggregation of the disease has been observed. HLA is a genetically
regulated molecule, which traps part of antigens and presents them on the
surface of cells for destruction by anti bodies and T-cell. It is designed to
recognize self from non –self cells. Researchers have identified a number of
HLA generic forms called HLA – DRB1 alleles. Which are referred to as the RA
shared epitope because of their association with RA.

6.  Climate: In the past it was thought that Rheumatoid arthritis was most
common in temperate zones, and was particularly associated with cold and
dump.
 Infection : A number of claims have been made that mycoplasmate and
diphtheroids have been identified with in rheumatoid synovial cells, the
role of these groups of organisms in etiology remains unproven.
Cigarette smoking
 Psychological factors : Psychological stress causes first attacks as well as
relapses. These also play a major role in the manifestation of disease.
(Nollander 1944)

7. Nutritional or metabolic factors: Intensive search has been made
in an effort to uncover a nutritional or metabolic fault in
Rheumatoid Arthritis. Patient with this disease often lose weight
and may present evident of nutritional deficiency, especially of
vitamin B complex.
 Super antigen driven diseases: super antigens are the proteins
produced by number of microorganisms like staphylococci,
streptococci etc. They have capacity to bind to HLA -DR molecule
and particular VB gene products. (Harrison) Recently scientists
have reported that smoking tobacco increasing the risk of
developing Rheumatoid Arthritis.

8. CLINICAL FEATURES :
 Prodromal Symptoms of Rheumatoid Arthritis :
 Joint swelling by several weeks.
 Morning stiffness, fatigue, anorexia, generalized weakness.
 vague musculoskeletal symptom like pain, weight loss,
malaise, myalgia, parasthesia

9. CLINICAL PRESENTATION AND SYMPTOMS:-
There are 7 types of presentation of R.A. They are as below,
1. Classical: - Pain, stiffness and swelling of small joints of upper limb
and lower limbs . Symptoms fluctuate in severity from day to day.
2. Palindromic: - Intermittent episodic form of inflammatory arthritis –
it means the joints pain and swelling on joints comes and go .Between
that attacks ,the symptoms disappear and the affected joints go back to
its normal condition, with no lasting more damages.

10. 3. Systemic: - Weight loss, pleurisy and pericarditis with minimal
joints involvement.
4. Polymyalgic: - Inflammatory disorder causing muscle Pain
and stiffness around shoulders and hips with subsequent
synovitis.
5. Monoarthritic: - Single joint involvement at a time, usually
knee joint.
6. Acute onset: - Sudden overnight onset with stiffness and pain.
7. Generalized lymphadenopathy.

11. • CRITERIA FOR DIAGNOSIS: As per American Rheumatism
Association- A.R.A. (1988)
• Morning stiffness - Stiffness of joints lasting up to one hour before
maximal improvement.
• Arthritis of three or more joints areas- At least three joints observed
by the physician, having pain with soft tissue swelling or joint
effusion, not only just bony over growth are included and the 14
possible joint areas ( R or L) have same features.

12. • Arthritis of hand joints -At least 1 area in wrist like M.C.P. or P.I.P is
swollen
• Symmetrical arthritis- Bilateral involvement.
• Rheumatoid nodules- Subcutaneous nodules over bony prominences.
• Rheumatoid factors - By any method that has been +ve in <5% of
normal subjects.
• Radiological changes - On PA view of hand & wrist radiograph that
must include erosions or unequivocal bony decalcification, localized in
or adjacent to involved joints.

13. EXTRAARTICULAR MANIFESTATIONS :
No. System Involved Features
1. Systemic Fever, fatigue, weight-loss, susceptibility to
infection.
2. Musculoskeletal Muscle-wasting, bursitis, tenosynovitis,
osteoporosis.
3. Hematological Anaemia, eosinophilia, thrombocytosis.
4. Lymphatic Splenomegaly, felty’s syndrome.
5. Nodules Sinuses, fistulae

14. 6. Ocular Episcleritis, scleritis, scleromalacia, keratoconjunctivitis sicca.
7. Vasculitis Digital arteries, ulcers, pyoderma gangrenosum, mononeuritis
multiplex, visceral arterities
8. Cardiac Pericarditis, myocarditis, endocarditis, conduction defect, coronary
vasculitis, granulomatous aortitis
9. Pulmonary Nodules, bronchiolitis, pleural effusions, fibrosing alveolitis,
caplan’s syndrome
10
.
Neurological Cervical cord compression, compression neuropathies,
mononeuritis multiplex, peripheral neuropathy.

15. pathology
joint inflammation is
immunologically
mediated.
In a genetically,
by activation of helper T-
cells responding to some
arthritogenic agent possibly
a microbe,
the activated CD4 cells produce a
number of cytokinines that produces
two principal effects.:-

16. 1) Activation of
macrophages and
other cells in one
joint space
release tissue
destructive enzyme
and other factors
that perpetuate
inflammation.

17. 2) Activation
of the B cell
system,
resulting in
the
production of
antibodies,
some of
which are
directed
against self-
constituents.
The resultant
autoimmune
reactions
damage the
joint
play an
important
role in
disease
progression.

18. destruction of bone, cartilage, fibrosis, ankylosis.
other enzymes causes Panus formation
Joint injury causes Release of collagenases, PGE2 &
Chondrocytes Proliferation
Cytokines causes Immune complex formation and deposition of Fibroblasts in
Synovial cells
Formation of R.A factor
Macrophage activation
T Cells and B Cell activation
Cytokines CD4
Antigen Microbe MHC Class II (Genetic susceptibility)

19. INVESTIGATION
• CBC
• ESR
• RF
• CRP-C REACTIVE PROTEIN
• ANTI CCP-ANTI CYCLIC CITRULLINATED PEPTIDE
• ANA-ANTINUCLEAR ANTIBODY

20. DEFORMITIES IN RHEUMATOID ARTHRITIS:

21. FEATURES ASSOCIATED WITH POOR PROGNOSIS:Greater number of
joints affected.
• Uncontrolled polyarthritis.
• Structural damage/ deformity (e.g. erosions of joints).
• Functional disability.
• High titre of serum rheumatoid factor.
• Presence of extra articular features (e.g. nodules).
• Psychological problems like stress , anxiety , depression etc. wit poverty, low
educational achievements, employment requiring heavy labour.
• Presence of HLA-DR4, particularly homozygosity.
• Positive family history.

22. DIFFERENTIAL DIAGNOSIS:
A. Gout: - In pathological investigation high serum uric acid level is present.
Response to administration of Colchicine is found in this condition.
B. Rheumatic Fever :- First, attacks are usually under 15 years of age in
70% of case. It is characterized by flitting type of joint pain and sustained
fever. Spindling of finger joint is rare. Myocarditis, endocarditis and nodules
on the different histological picture are present.
C. Polymyalgia Rheumatica :- In this condition ESR is very high and
peripheral joint signs are minimal. (Onset of Rheumatoid Arthritis in elderly
mimic Polymyalgia Rheumatica)

23. D. Polyarthritis Nodosa: - May resemble Rheumatoid Arthritis, but
radiological changes are minimal. Severe systemic symptoms and necrotizing
vasculitis at early stage of polyarthritis may be present, but joint erosions and
typical Rheumatoid Arthritis deformity are rare in later stage.
E. Osteoarthiritis:- This occurs in older people with the complete lack of the
systemic features of R.A. such as fever, weight-loss, fatigue etc. The duration of
morning stiffness, joint swelling, are less compared to R.A. Radiological
appearance differs, absence of subcutaneous nodules and R.A. factor. In typical
case, Heberden's nodes appear in relationship to DIP joints and ESR usually
within normal limits. Mostly weight bearing joints are affected first.

24. F. Systemic Lupus Erythematosis: -The joint involvement are not
symmetrical nor are ankylosis and erosions common. It is characterized by
the presence of numerous auto antibodies, circulating immune complexes
and widespread immunologically determined tissue damage.
G. Psoriatic arthropathy:- Characteristic skin and nail lesions may be
present. The D.I.P. joints are usually involved. The R.F is negative.

25. ASSESSMENT IN RA
VAS SCALE ASSESSMENT:
DAS 28 SCALE ASSESSMENT:
1. joint count tenderness(28):
2. joint count swelling (28):
3. CRP mg/L:

26. DISABILITY INDEX (the Indian health assessment questionnaire)
Sr.No Activity of daily living (ADL) are you able to:
1 Dress yourself, including tying saree/salwar/dhoti and doing buttons?
2 Get in and out of bed?
3 Lift full cup or glass to your mouth?
4 Walk outdoors on flat ground?
5 Wash and dry your entire body?
6 Squat in the toilet or sit cross-legged on the floor?
7 Bend down to pick up clothing from the floor?
8 Turn a tap on and off?
9 Get in and out of auto rockshaw/car?
10 Walk3 kilometers?
11 Shop in the vegetable market?
12 Climb a flight of stairs?
Disability Index= Sum of all scores/12

27. TREATMENT:
General Principles: The goals of therapy of RA are
(A)Relief of pain,
(B) Reduction of inflammation,
(C) Protection of articular structures,
(D) Maintenance of function and
(E) Control of systemic involvement.

28. Pharmacotherapy:
(a)Non steroidal anti-inflammatory drugs (NSAIDs): NSAIDS have no
effect on long term disability but provide symptomatic relief like in pain
and stiffness.
(b) Glucocorticoid therapy:Used to suppress signs and symptoms of
inflammation
(c) Disease-modifying antirheumatic drugs (DMARDs): The onset of
effect is usually delayed (4 weeks to 3 month) and they have various
mechanism of action. They can alter laboratory markers of
inflammation such as ESR and CRP.
-methotrexate,sulfasalazine

29. (d) Anti-cytokine agents: major impact on the signs and
symptoms of RA and also to slow progressive damage to
articular structures.
(e) Immunosuppressive therapy
(f) Anti TNF Therapy

30. Non-Operative methods:-
Physiotherapy
Occupational therapy
 Rehabilitation :the patient with the help of devices like braces,
walking-aids etc.
Operative Methods
Preventive Surgery
Palliative Surgery
Reconstructive Surgery

31. AYURVEDIC REVIEW

32. Concept of ama
• As the term indicates, “Amavata”
Ama+Vata
• In Ayurvedic classics, Ama which is the product of metabolic defect it
has been considered an important factor for the pathogenesis of the
most of the diseases. It is essential to see the presence or absence of
Ama in a patient before starting the treatment, because the line of
treatment is totally different in case of Samavastha (presence of Ama)
and Niramavastha (Absence of Ama).

33. DERIVATION:
The word Ama is derived from
Am raegexatu + Aa + x<g àTyy (A.K) - here the presiding vowel is elongated and word
“Ama” is formed.
According to Hemchandra, Gatyartha Ama Dhatu + Nich Pratyaya = Ama
VYUTPATTI:
AaMyte $zt! pCyte,, AaMyte gMyte pKvadxR< #it Aam>, (Amarkosh)
Underwent slight Paka or which is half digested or which is detrimental to
Strotas.
AaMyte ip*te ôaetasmhUa Anneeit Aam>, (Amarkosh)

34. • A product which is homologues in nature is likely to produce
no discomfort. On the contrary if any substance is not
congenial to Strotas, it may harm them like Ama. Substance
which is detrimental to Strotas is termed as Ama. It produces
pain or creates pressure on srotomukha and accumulates in
Srotomukha.

35. VARIOUS DEFINITIONS OFAMA :
• jQranldaEbRLyat AivpKvStu yae rs>, s Aams<¶kaedehe svRdae;àkaep[>. (Madhukosh)
• ¢h{ya< pCyte kaeóviûna Jaayte kqu>,rsae Évit sMpKvadpKvadam s<Év>, (Sh.Pu.Kh.6/7)
AMA NIDANA:
1.Aaharajanya
2.Viharajanya
3.Manasika
4.Others

36. (1) Aharajanya (dietetic indiscretions)
AÉaejnadjI[aRitÉaejnadiv;maznat,
AsaTMy<guézItaité] s<ÊòÉaejnat.(cha.chi.15)
(2) Viharjanya:-
ATy<MbupanaiÖ;maznaScsNxar[atSvßivpyRyaSc,(shu.shu.15)
(3) Manasika Bhava:
maÇaya=Py_yvht<pWy<caÚ<njIyRitic<tazaek Éy³aex Ê>ozYyaàjagrE>.
(4) Others:
ivrekvmn<õehivæmadVyaixk;R[at!,
dezkaltu vE;Myadvegana< civxar[at!.(cha.chi.15)

37. AMA SWAROOPA:
अविपक्िमसंयुक्तं दुर्गन्धं बहुवपच्छिलम्| सदनं सिग र्ात्राणाम् ममम् त्यिधधययत||
(a.h.su.15)
Ôv<guvRnekv[¡hetu> svRraega[a<iõGx<ipiCDlmam<tNtumdnubÏzUl< ÊgRiNx #Tyaid,
Classification of formation of Ama
1. Ama produced by Agnimanadya.
(i) Ama produced by Jatharagnimandya.
(ii) Ama produced by Bhutagnimandya and Dhatvagnimandhya.
(iii) Mala Samchaya Rupa Ama.

38. 2. Ama produced independent of Agni –
(i) Ama produced as the first stage of Doshika vitiation.
(ii) Ama produced by ingestion of poison or other
external factors.
(iii)Prathma Doshadushti Janya Ama.

39.  Ama Samanya Lakshana-
öaetaeraex bl æ<z gaErvainl mUFta,
AalSyapi´ in:QIv>mls¼aéic¬m>,(ma.ni.25)
 il¼< mlana<samana<,inrama[a< ivpyRy>,(A.H.Su.13/24)

40. MODERN CONCEPT OF AMA:
• The term “Ama’’is not a single entity but it can be applied to many
malformed substance in the body. Ama when we speak about Sthoola
Ama at the level of Jatharagni it could be easily understood as
undigested food due to weakness of digestive power. But when we
speak about Sookshma Ama at the level of Dhatu the answer is not
so easy to be understood.

41.  Various malformed substances can be compared with Ama.
Impaired protein metabolism: uric acid.
Impaired fat & carbohydrate metabolism: lactic acid, ketone
bodies, ketones
Incomplete metabolism of Hb: methaemoglobin.
Bacterial action: indol, sketol, methane, hydrogen sulphide etc.
Incomplete process of bile leads to discolorations of stool.

42. ETIOLOGICAL FACTORS OF VITIATION OF VATA
Ahara: Ruksha, Sheeta, Alpa, Laghu, Abhojana
Vihara: Vyavaya, Atiprajagarana, Vishama Upachara, Dosha-Rakta
Atistravana, Langhana, Plavana, Atyadhva, Vyayama, Ativichesta,
Dukkha,Sayya Aasana, Divaswapa, Vegavidharana, Abhighata,
Marmaghata, Patana.
Manasika: Chinta, Shoka, Krodha, Bhaya.
Miscellaneous: Dhatu Kshaya, Rogatikarsana (emaciation due to
disease)

43. CLASSIFICATION OF VATA:
No
.
Name of Vayu Normal Function Vitiation in Amavata
1. Prana Vayu:
Located at Head,
Chest, Throat,
Tongue and Mouth
Shteevan, Kshavathu, Udgar, Shwasa, Budhi
Hrudaya Indriya Chitta Dharana
Praseka,
Shirshula,
Murchha etc
2. Udana Vayu:
Located at Chest,
Umbilicus,Throat
Vakapravrutti, initiation of body activity, enthusiasm,
strength, lustier,Prayatna mediates Chesta, grasping
power, knowledge, memory,stimulation of mind.
Chhardi etc.

44. 3. Samana Vayu:
Located in Sweda-
Ambuvaha Srotas and
seated beside
Ámashayastha Agni
Influences the Srotsas of Doshas,
Mala, Shukra, Artava and Ambu. Strengthens Agni
Annadharana, Pachana & Vivechana, Sara Kitta
Vibhajana. Dosha, Mala, Shukra,Artava, Ambuvaha
Srotovichari
Agnimandya
Ama formation
Etc.
4. Vyana Vayu:
Located at Hridaya
and Sarvasharira
Performs movements, Rasa Vikshepana, Prasarana
Akunchana (contraction & dilatation of vessels),
Nimesh-Unmesh (opening &closing of cardiac valves) Anna
Swadana, SrotoShodhana, Sandhi Samshleshana etc.
Sandhigraha,
Sandhishoola,
Sandhishotha,
Angamarda
etc.
5. Apana Vayu:
Located at Nabhi,
Bladder, Intestine,
Testicle, Thighs Penis,
Elimination of faeces, flatus, urine, Shukra, Artava & foetus
etc.
Vibandha,
Bahumutrata,
Aantrakujana
etc.

45. AMAVATA
Derivation Of Amavata :
ममन सहहतो िातः ममिातः |
• A condition wherein Ama gets associated with Vata dosa is Amavata
ममं च िातं च ममिातम् |
• Association of Ama &Vata collectively forms the term Amavata

46. • Definition :
युर्प्कु वपतािन्तच्रत्रक्सच्न्धप्रिशकौ |
रतब्धं च कु रुतो र्ात्रमामिात स उछयत || (Ma.Ni-25/5)
There is simultaneous aggravation of Vata & Kapha dosha within the
Koshtha & after Vimarga gamana enter into Trik Sandhi & result into
Gatra Stabdhata & that is called as Amavata.
It means inability to perform the karma (bending movement) by the
Affected joints

47. Classification of Amavata
(1) Acc. to Dosha involvement
• Ek Doshaja: - (1) Vataja (2) Pittaja (3) Kaphaja
• Dvandvaja: - (1) VataPittaja (2) vatakaphaja (3) pittakaphaja
• Sannipataja: - Vatapittakaphaja
(2) Acc. to severity:
• (1)Samanya Amavata (2) Pravrudha Amavata
(3) Acc. to prognosis/chikitsa parinama:
• (1)Sadhya-Eka Doshaja (2) Yapya-Dvi Doshaja (3) Kricchrasaadhya-
Sannipatika

48. NIDANA PANCHAK:
1.NIDANA :
(A)Viruddha Aahara
(B) Viruddha Cheshta
(C)Manasika
(D) Others – (i) Mandagni
(ii)Nischalatva
(iii)Nidanarthkara Vyadhi

49. (2) PURVARUPA:
Acharya Bangasen has given Shiroruja and Gatraruja as Purvarupa of
Amavata.
 According to some Vaidyas Angamarda, Aruchi etc. Lakshanas of
Samanya Amavata are actually the purvarupa of Amavata &
Lakshanas described as Pravrudha Amavata are the actual symptoms
of the disease.
 According to “concept of Ama in Ayurveda” by Dr. Srinivasulu--
Janyet Ashu Daurbalyam + Gauravam Hridayasya Cha are the
Purvarupa of Amavata.

50. (3) RUPA :-
The signs and symptoms of Amavata can be classified under the four
captions:
(1) LAKSHANA (Cardinal & Associated Symptoms)
(2) VISHESH LAKSHANA (Dosha wise Symptpms)
(3) PRAVRIDDHA AMAVATA LAKSHANA (Aggrivated symptoms)

51. (1) Lakshana:
A<gmdaeRféicSt:&[aAalSy<gaErv<Jvr>,
Apak>zUntaf<ganamamvatSyl][m!. (Ma.ni.25)
(2) Vishesha Lakshana:
ipÄaTsdahrag— cszUl—pvnanugm!,
iStimt<guék{fªck)Êò—tmaidzet!.(Ma.ni.25)

52. (3) Pravriddha Amavata Lakshana:
kò> svRraega[a< yda àki…ptae Évet!,
s dezae éJytefTyw¡ VyaivÏ #v v&iíkE>.
jnyet saefi¶daEbLRy< àsekaéicgaErvm!,
%TsahhainvErSy <dah< c bहुmUÇtam!.
t&q DidR æm muCDaRí ýd¢h< ivfivbÏtam!,
jaf(aÙkªjmanah<kòa<íaNyanupÔvan!.(Ma.ni.25)

53. (4) UPSHAY-ANUPSHAYA:
Upshaya:
Ruksha Swedana:
 Langhana, Upavasa, Pipasa, Atapasevana, Pachana all are helpful measures for
Upashaya of Amavata.
Anupshaya:
Sheeta, Snigdha, Guru Aahara adds to the suffering of patients.
Tailabhayanga

54. (5) SAMPRAPTI:
ivéÏaharceòSy mNda¶einRílSy c,
iõGx< Éu´vtae ýÚ< Vyayam< k…vRtStwa.
vayuna àeirtae ýam> ðe:mSwan< àxavit,
tenaTywR ivdGxaefsaE xmnI> àitpXyte.
vat ipÄ k)EÉURyae Êi;t> saefÚjae rs>,
ôaeta<SyiÉ:yNdyit nanav[aeRfitipiCDl>.
jnyTyaz udaEbRLy< gaErv< ÿdySy c,
Vyaixnamaïyae ý;eAams<¶aefitdaé[>.
yugpTk…iptavNt iÇksiNxàvezkaE,
StBx< c k…étae gaÇmamvat> s %½te. (Ma.ni.25)

55. UPDRAVA :
(1) In Anjana Nidana 8 Updrava of Amavata are mentioned
Jaaf(aÙkªjnanaht&qCœDidRbहुmUÇtam!,
zUl< zynnazae=òaepÔvaAamvatj>.
2) According to Madhukosha commentary upon Madhava
Nidana Updrava refers to Sankocha & Khanja .
3) according to Harita.
A¼vkELyamayait Aamvate iÉ;Gvr>.

56. SAPEKSHA NIDANA:
AMAVATA SANDHIVATA
1)sama + -
2)jwara + -
3) symptoms of Ama So many No symptom
4)Type of Vedana Vrushchika Damshvata
Vedana
Samanya Shoola
5)Pain All time pain Pain during Prasarana &
Akunchana
6)Apply taila abhyanga Pain increases Pain decrease
7)Pain relieved with Deepana and Pachana Brumhana and Snehana

57. AMAVATA VATARAKTA
1) Simultaneous
consumption of
Ama Janaka & Vata Prakopaka
Nidana
Vata Prakopaka & Rakta
Prakopaka Nidana
2) Shoola Pain and swelling in joints Pain and swelling in
joints
3) Dosha Vata & Kapha Vata & Rakta
4) Dushya Rasa Rakta
5) Ama Ama predominance Not so predominancy of
Ama

58. 6) Jwara Jwara is PradhanaLakshana Jwara is not Pradhana
7)Rakta Dushti Rakta Dushti is not present Rakta Dushti is present
8) Sthana Kapha Sthanas, Sandhis Hasta & Pada Sandhis
9) Strotas Rasavaha Raktavaha
10)Snehana Pain increase Pain decrease
11)Raktamokshana Not as a treatment As a treatment
12)Ushna Chikitsa Relieves the symptoms May provoke the symptoms
by Rakta Vidahana

59. AMAVATA KROSTUKA SHIRSHA
1)Shoola Pain and swelling in joints Pain and swelling in Knee joint
2)Lakshanas Rasa Dushti Lakshana Raktadushti Lakshanas
3) Sandhis More Sandhis affected Only knee joint affected
4)Dushya Rasa Dhatu Rakta Dhatu
5)Appeareance Spindle shaped fingers A characteristic resemblance of the
affected joint with the head of
jackal.

60. CHIKITSA OF AMAVATA:
l<"n< Svedn< it´< dIpnain kqunI c,
ivrecn< õhepan< bStyíammaéte.
sENxva*enanuvaSy]arbiSt> àzSyte.
Aamvate pÁckaelisÏ< panaÚim:yte,
é]> Sved> àktRVyaebalukapuqkEStwa.

61. THANK YOU