1. Shree Ganeshaya namah

2. WELCOME WELCOME 3. RAJAYAKSHMA TUBERCULOSIS 4. Shree Ganeshaya Namah.. 5.

A Seminar by: Sandeep kumar sharma

Guided by: Dr.Samir Bhadri

HOD in maulika siddanta

SDAC Siddapur (N.K.)

6.

Dedicated to my

respected Father and

mother..

7. Acc. to Ayurveda 8. Synonyms

:

: :( . . . / )

9.

Rajayakshma:Because King Chandra suffered this disease first time.

Kshaya : It Diminishes strength and activities.

Sosa : Because it dries up Rasadi dhatus.

Rogarat : It is a powerful disease. It is a disease which is very difficult to treat.

10. King Chandra married 28 daughters of Dakshaprajapati but unable to satisfy all except Rohini as he was more interested in her. So remaining complaint to their father and Daksha Prajapati became furious and his anger came out of his mouth through expiration and King Chandra suffered by Rajayakshma. Mythological history (charaka s.chi.8/3-12) 11. Due to occurrence of disease first time in Raja so called as Rajayakshma. 12. Hetu

;

- , ( . . .6/3 )

(c.s.ni.6/3 and s.s.u.41/9) 13. 1) Sahasa or (over exertion) 2) Sandharana (suppression of natural urges 3) Kshaya (wasting) 4) Vishamashana (irregular dieting) There are four etiological factors Acc. To charaka 14. : :( . . .41/9 ) 15. There are four etiological factors acc. To susruta

Khsaya

Vega pratighata

Aaghata

vishamaashana

16. When a person does the work which is out of his capacity is called as Sahasa. Acharya Charaka mentioned different examples of Sahasa like: 1.Sahasa or aaghataja 17.

- when a week person fights with a stronger person

- perform exercise with big bow

- speaks too much

- carries over weight

- swims for longer distance

- subjected to forceful anointing therapy

application of pressure by feet

- running fast for longer distance.

- Practices such other irregular regimens and physical exercise in excess.

. 18. Samprapti

As a result of these factors his chest becomes wounded

the wounded chest gets saturated with Vata

brings abnormality in both Pitta and kapha

spreads upwards, downwards and sideways.

19.

Due to injury to chest, patient constantly suffers from coughing due to irregular movement of Vata and irritation of throat.

Frequent coughing leads to Haemoptysis and weakness and causes Rajayakshma.

20. Lakshanas

These vitiated doshas after entering the sandhis (joints) cause:

Jrambha (yawning),

Angamarda (Pain in body parts) and

Jwara (fever).

21.

After entering the Amashaya causes:

Uro-roga (chest disease)

Arochaka (anorexia)

After entering the Kantha (throat) causes:

Kanthodhwamsa (irritation of throat)

Swara bheda (hoarseness of voice)

22.

After entering the Pranavaha srotasas causes:

Swasa (dyspnoea)

Pratishyaya (rhinitis)

After entering in head produces:

Sira shula (distress in head)

23. 2)Sandharanaja or vega pratighataja(Suppression of natural urges)

Due to suppression of natural urges of Apana vata, mutra (urine) and mala (flatus) because of:

Attending the king or master

At the feet of the Guru

While gambling

24.

Attending meetings of gentleman

Stree madhye (in b/w ladies)

While travelling on uneven vehicle

Bhaya (Due to fear)

Prasanga or during Maithuna

Lajja

Ghruna (badboo utpanna hone ke dar se)

25. Samprapti ofsandharana janya Rajayakshma

Due to above mentioned factors the Vata gets vitiated

abnormality in Pitta and kapha

after this vata moves downwards, upwards &sideways

produces different symptoms.

26. Lakshanas of sandharana janyaRajayakshma

Shula (abdominal pain)

Mala bheda (atisara) or hardness of stool

Pain in ribs or sides of the chest, shoulder

Irritation in chest and throat

Headache

cough

Dyspnoea

Fever

Hoarseness of voice

27. 3. Kshaya hetu

Anuloma kshayaja hetus:

Excessive shoka (grief), chinta (worry), Irshya (envy ness), Utkantha (anxiety), Bhaya, Krodha afflicts heart.

Ruksha aahara

Alpahar (less intake of food)

Anahar (excessive fasting)

28.

All above etiological factors leads to Rasa dhatu kshaya which leads to manifestation of sosa Roga.

Delay in management causes Rajayakshma.

29. Pratiloma kshayaja Hetu

Ati Maithuna

30. - Ati Maithuna leads to Shukradhatu kshaya - after Shukra kshaya if person indulges in sexual activity - no semen ejaculation - vata enters the blood vesselsand causes blood dischargehaving vata gunas from seminal passage. Samprapti of kshaya janya Rajayakshma 31.

vitiated vata spreading the entire body and aggravates Pitta and kapha

Pitta dries up the mamsa and rakta

leads to sosa

leads to Rajayakshma

32. Lakshanas

Pain in the side of the chest and shoulders.

irritation in throat

Angamarda

Aruchi

Indigestion

Jwara, kasa, swarabhada, pratishyaya (due to pratiloma vata)

33.

Excess kasa leads to sputum along with rakta and due to rakta kshaya further dhatu formation stops and person becomes weekend and leads to Rajayakshma.

Thats why one should protect his Shukra dhatu.

34. Vishamashana hetu

Ifthe person adopts unhealthy dietetic pattern will lead to Rajayakshma.

35. Samprapti of vishamashanaja Rajayakshma

When a person does pana, ashana, bhakshya, lehya upayoga opposite to the prakruti, karan, desha, kala, upayoga samstha and upashaya then his doshas get vitiated

these vitiated dosha obstructs the srotasas

maximum part of the food turns into pureesh and mutra

no rasadi dhatu formation

Sosa

Leads to Rajayakshma.

36.

Here vitiated Vata leads to:

Shula

Angamarda

Kanthodhwamsa

Parshva samrujan

swarabheda

pratishyaya

37.

Here vitiated Pitta leads to:

Jwara

Atisara

Antardaha

38.

Here vitiated kapha leads to:

Pratishyaya

Aruchi

Kasa

Siraso gurutvam

39.

In this case one should do pureesh rakshana because pureesh is the one which supports the body.

If a person suffers from constipation then he will not suffer so much but if he is having atisara then it will suffer him more.

40. Samprapti of Rajayakshma

: : :

( . . .41/9-10 )

41. Samprapti: Acc. To susruta

Due to obstruction in rasavaha srotasas due to kapha or

indulging more in maithuna leads to depletion of rasadi dhatus due to shukra kshaya and leads to Rajayakshma.

42.

: :

( . . .5/5-6 )

43. Sampraptiacc. To Vagbhata

Aggravated vata produces increase of both pitta and kapha

and spreads to all joints of the body and through siras goes upwards, downwards and sidewards and obstructs or dilates the srotasas and manifests Rajayakshma.

44. Rajayakshma Samprapti ghatakas

Dosa : kapha pradhana tridoshas

Vata (vyana, samana, udana, prana andapana)

Pitta (pachaka and sadhaka)

Kapha (kledaka, bodhaka, avalambaka)

Dushya : Dhatus (rasa, raktadi all Dhatus)

Upadhatus (sira and sandhi)

Sharirika mala (mutra and pureesh)

Dhatu mala (kapha, Pitta, sweda, kasha, loma, nakha)

45.

Agni : Jatharagni, dhatwagni, bhutagni

Agnidusti : mandata

Ama : tad Agni janya Ama

Srotas : annavaha, rasavaha, shukravaha mainly

Rasavaha (anuloma)

Shukravaha (pratiloma)

Later all the srotasas gets obstructed.

46.

Srotodusti : sangha and vimarga gamana

Udbhava sthana : amashaya and pakwashaya

Adhisthana : sarva sharira

Vyakta sthana : mukha and sarva sharira

Sanchara sthana : rasa vahinis

Svabhava : chirkari

Roga marga : madhyama

47. Sadhya asadhyatva

Sadhya in strong person

Asadhya in weak person

48.

:

: :

:( . . .8/33-36)

49.

: :

:

( . . .41)

50. Purvarupas

Pratishyaya

Dorbalya

Stree madya mamsa priyata

Frequent sneezing

Excess salivation

Sweet taste in mouth

Aversion towards food

Feeling of exhaustion during meal time

Swelling on the face and feet

51.

Frequent looking at the hands

Excessive whitishness of eyes

Swasa

Angamarda

Talushosa

Vamana

Agninasha

Mada

Nidra

52.

In dreams he sees:

Empty reservoirs

deserted villages, towns, cities and countries

dried, burnt, and destroyed forest.

Riding over dog, camel, donkey and pig etc.

53.

: : ( . . .41/15)

jwara

kasa

haemoptysis

54. Acc. To charaka

: :

: :

:

: :

: : : :

: ( . .8/45-47)

55.

kasa

santapa or fever

vaiswarya ( derangement of voice)

parshva shiro ruja

diarrhoea

Aruchi (anorexia)

56. Acc. To susruta

: : :

( . . .41/5)

57.

bhakta dwesha

jwara

Swasa

kasa

rakta shtheevana

swarabheda

58. Acc. To charaka

,

- : , :, :,

:, , ,

, :, :, :, ( . . .6/14)

59.

shiras paripurnatwam

kasa

Swasa

swarabheda

vomiting of shleshma

shonita shtheevana (haemoptysis)

parshva ruja

ansavmarda

jwara

atisara

arochaka

60. Acc. to susruta

: :

:

:

: : :( . . .41/6-7)

61. Due to vata

Swarabheda

Amsha parshva sankocha

Amsha parshva shula

62. Due to Pitta

jwara

daha

atisara

rakta shtheevana

63. Due to kapha

heaviness of head

Aruchi

Kasa

Kantha peeda

64. s

( . . .41/13)

without fever

balwaan

kriyasahya

deeptagni

akrish

65. s acc. to charaka

, ,

; ,

( . . .6/16)

66.

Durbala

Ati ksheena mamsa, bala and rakta

Aushadha asahya

67. acc. to susruta

:

: :

:

: : :

:

( . . .41/8-12)

68.

One who is having all ekadasha rupas, shadrupas and trirupas along with loss of bala and mamsa

Atisara

Shoonmushkodara (swelling on testis and abdomen)

Shukla akshi

Anna dwesha

Urdhva Swasa

Painful micturation

Arista lakshanas are present.

69.

: :( . . .41/14)

70.

vyavaya

shoka

vardhakya (vriddhavastha)

vyaayama

aadhva

vrana

urakshata

71. Difference between sosa and Rajayakshma

Madhava has given difference between shosha and Rajayakshma.

There should be presence of jwara and dandanu in Rajayakshma but in shosha it is not compulsory.

72.

Rajayakshma can be called shosha any time but shosha can not be said as Rajayakshma every time.

Ex.

Shoka shoshi and jara shoshi will not be called as Rajayakshma peedita.

73.

:

Sitopalaladi churna

Durlabhadighrita

Jivantyadighrita

Talisadi churna and gutika

74. Acc. To modern science.. 75.

TUBERCULOSIS

Pulmonary 76. Some terms related to the topic

Hilar - related to hilum or hilus.

Lesions - discontinuation of tissues.

primary focus- thestarting point of disease process.

Tabes Mesenterica- a progressive wasting of the Intestine.

77.

Caseous - cheesy appearance

Erosion -destruction of tissue

milliary TB- acute or generalised TB.

Orthopnoea- discomfort in breathing in any position except sitting or standing position.

78.

Amyloidosis- it is disease in which amyloid is deposited extracellularly

Amyloid a glycoprotein resembling like starch

AFB- acid fast bacilli

Culture- to induce the propagation of micro organisms in special media which are promoting their growth.

Smear- a specimen for microscopic examination on slide.

79. Droplet infection

Droplet very small drop.

Spreading of infection by fine infected particles as by sneezing from the nose or by spitting from mouth.

80. Causative organism

Tubercle bacillus or Kochs bacillus orMycobacterium Tuberculosis.

Organismis a strict aerobe and lives in the part where theoxygen supplyis more,

Likeapex of the lungs .

Mycobacterium Tuberculosis Bovisis mainly a causative factor by theunpasturatedmilk from the animals.

81. Mycobacterium Tuberculosis hominis

slender rod like bacillus.

Neutral on gram staining.

It can be demonstrated by:

1) Acid fast or ziehl neelson staining.

2) Fluorescent dye methods.

3) Culture of organism in sputum.

82.

Tuberculosis is an infectious disease caused byMycobacterium tuberculosis . The disease primarily affects lungs and causesPulmonary Tuberculosis . It can also affect intestine, meninges, bones and joints, lymph glands, skin and other tissues of the body.

The disease also affects animals like cattle and known asBovine Tuberculosis .

83. Atypical or non tuberculous mycobacteria

Atypical term is used for the other species of Mycobacteria rather than Mycobacterium tuberculosis complex also called asenvironmental Mycobacteria.

84. Mode of transmission

Human beings acquire infectionwith tubercle bacilli by following routes:

1)Inhalation :from cough droplets or dried sputum from an open case ofPulmonary TB.

2) Ingestion :Leads to tonsillar or intestinal tuberculosis.

3)Incubation :From infected post-mortem tissue or through skin.

4)Trans placental route : Congenital Tuberculosis in foetus from infected mother.

85. Incubation period

Development of disease depends upon the closeness of contact, extent of disease andsputum positivityof source or dose of infection and host parasitic relationship.

Thus the incubation period may be weeks, months or years.

Normal incubation period - 3 to 6 weeks .

86. Spread of TB

1)Local spread :This takes place by macrophages carrying the bacilli into the surrounding tissues.

2)Lymphatic spread :TB is primarily an infection of lymphoid tissues. The bacilli may pass into lymphoid follicles of pharynx, bronchi, intestines, regional lymph nodes.

3)Haematogenous spread : Because of the drainage of lymphatics into vessel system.

87.

4)By the natural passages :

(A) Lung lesions into pleura

(B) Transbronchial spread into adjacent lung segments

(C) Into peritoneal cavity (tuberculousperitonitis)

(D) Infected sputum into larynx ( Tuberculous laryngitis )

(E) Swallowing of infected sputum ( illeocaecal tuberculosis )

(F) Renal lesions into ureter

88. Evolutionof tubercle

Tubercle bacilli invasion

lodges in pulmonary capillaries

due to tubercle bacilli coating ofopsoninwith in 12 hours progressive infiltration by macrophages occurs

phagocytosis by macrophages

activation of T&B lymphocyte cells

B cells produce antibodies but dont have any role in defence against tubercle bacillus

T helper cell(CD4+T) inactivation

89.

without T helper cell no immune system stimulation

formation of granuloma

Hard tubercle formation (due to absence of central necrosis)

central mass caseation (the process of conversion of necrotic tissue into cheesy material)

soft tubercle formation

Tuberculosis occurrence.

90. Types of Tuberculosis

Lungs are the main effected organ in TB. Depending upon the type of tissue response it is of two types:

1)Primary TB

2)Secondary TB

91. Primary TB

The infection of an indivisual who has not been previously infected or immunised is calledPrimary TBorGhons complexorchildhood TB.

Most probably involved tissues in Primary Tb are Lungs & hilar (related to hilum or hilus) lymph nodes.

Others are: tonsils, cervical lymph nodes.

In the case of ingestion of bacilli lesions (discontinuation of tissues) may be found in small intestine and mesenteric lymph nodes.

92. This type of TB consists of 3 components

1 )Pulmonary component :Leisons in the lung is the primary focus.

It is more often in the upper part of the upper lobe of the lung.

2)Lymphatic vessel component

3)Lymphatic component :Enlarged hilar and tracheobronchial lymph nodes.

93. Note :

In the case of Primary TB of the alimentary tract due to ingestion of tubercle bacilli a smallprimary focus(the starting point of disease process) is seen in intestine with enlarged lymph nodes producingTabesMesentrica(a progressive wasting of the Intestine).

The enlarged and Caseous mesenteric lymph nodes may rupture into peritoneal cavity and may causetuberculous peritonitis.

94. Fate of Primary TB

1) The lesions of lung may not progress but instead of healing byfibrosis, calcificationandossificationmay occur.

2) Primary focuscontinues to grow and Caseousmaterial is sent to the other part of the same lung or to another lung. It is called asProgressive primary TB.

3) Bacilli may enter the circulation througherosion ( destruction of tissue) in blood vessels and may spread to various tissues and organs. Thisis calledPrimary milliary TB.

4) Healed lesions of primary TB may be reactivated. It is calledProgressive secondary TB.

95. Secondary Tuberculosis

Infection ofan individual who has been previously infected is called secondary or post primary or reinfection or chronic TB.

The infection may be acquired from:

(A)Endogenous source:such as reactivation of primary complex.

(B) Fresh dose of reinfection by tubercle bacilli.

96.

Secondary TB occurs mainly in apex of the lungs.

Other sites of infection are tonsils, pharynx, larynx, small intestine and skin.

97. Fate of sec. pulmonary TB

(A) Lesions may heal with fibrosis and calcification.

(B) Lesions may join together to form larger area to involve in disease.

(C) Fibrocaseous TB

(D) Tuberculous caseous pneumonia

(E) Milliary TB

98. HIV associated tuberculosis

HIV infected individuals are more prone to get TB and vice versa.

Rate of HIV infection in TB patient is very high.

Extra pulmonary TBis more common inHIV patients.

99. Clinical features

The clinical manifestations in tuberculosis may be variable depending upon the location, extent and type of lesions.

Usual clinical features are as under:

100. Referable to lungs

Productive cough may be with blood(haemoptysis)

Pleural effusion

Dyspnoea

Orthopnoea(discomfort in breathing in any position except sitting or standing position)

Chest X-ray may show Nodularity.

101. Systemic features

Fever

Night sweating

Fatigue

Loss of weight and appetite

Note:Untreated cases may developsystemic secondary amyloidosis .

102. Diagnosis

Tuberculin :The test material or antigen is known as tuberculin. It is of two types:

(a) Old tuberculin(OT)

(b) Purified protein derivative(PPD)

PPD has replaced OT due to its standardization in terms of its biological reactivity astuberculin units(TU).

For routine testing - 1 TUdose is used.

103. Milliary TB

This disease is the result of acute diffuse tubercle bacilli via bloodstream.

It is difficult to diagnose.

Because chest X-ray may be entirely normal

Mantoux test may also be negative.

104. 1. Mantoux test

It is carried out by injecting1 TU of PPD in 0.1 ml on the flexor surface of forearm intradermally.

WHO advocatesPPD-RT-23 with tween 80preparation for testing.

Result is read out after 72 hours of injection by seeing the diameter of induration.

105.

If the diameter is more than 10mm thenPositive case tests .

If the diameter is less than 6mm thennegative case test.

If the diameter is in b/w 6 to 10 mm then doubtful case test.

106.

2. Positive sputum for AFB (on smear or culture)

3. complete haemogram ( lymphocytosis )

4. Chest X-RAY

5. Fibreoptic bronchoscopy

6. Biopsy

107. Causes of death in Pulmonary TB

Pulmonary insufficiency

Pulmonary haemorrhages

Sepsis (presence of micro organism in blood)

Cor pulmonate orsecondary Amyloidosis .

108. Prevention or vaccination

It is done by BCG(baccilae calmette Guerin)vaccination.

It is of two types:

A. liquid or fresh vaccine

B. freeze dried vaccine

109. Dosage

Usual strength is 0.1mg in 0.1ml volume.

In newborn baby below 4 weeks is 0.05 ml.

Should be given at birth or at 6 weeks if not given at birth.

Given intradermally.

110. Treatment

Treatment given in TB is called aschemotherapy , which is having drugs of:

highly effective

free from side effects

easy to administer

reasonably cheap

111.

Currently used drugs may be classified in to two groups:

Bactericidal : These drugs kill the bacilli in vivo.

Bacteriostatic:Inhibit the multiplication of the bacilli and lead to their destruction by immune mechanism of the host.

112. The three basic conceptsin TB treatment are as follows:

Regimens must contain multiple drugs to which the organism is susceptible.

Drugs must be taken regularly.

Drug therapy must continue for sufficient time.

113. Antituberculous drugsare classified as.. 114. Firstline antituberculosis drugs

Superior in efficacy and posses an acceptable degree of toxicity. these are:

Isoniazid, rifampin, pyrazinamide, ethmabutol, streptomycin.

115. Isoniazid

Mechanism of action: It inhibits the synthesis of mycolic acid (an essential factor for the formation of mycobacterial cell wall synthesis)

no growth of tubercle bacillus further.

116. Rifampin

Mechanism of action:

It inhibits the DNA synthesis

no further growth of tubercle bacilli.

117. Pyrazinamide

It is well absorbed from GIT

penetrates tissues, macrophages, tuberculous cavities.

It has excellent effect on intracellular mycobacteria due to acidic environment.

Half life: 9 to 10 hours.

118. Ethamabutol

• It also inhibits the DNA synthesis.

Half life: 3 to 4 hours.

119. Streptomycin

Bactericidal.

120. Second line antituberculosis drugs .. 121. Second line antituberculosis drugs

More toxic and less effective and they are indicated only when organisms are resistant to the first line agents. They are:

Cycloserine, ethionamide, aminosalicylic acid, rifabutin, quinolones, capreomycin, viomycin and pyridoxine.

122. Para-aminosalicylic acid (PAS)

It is a Bacteriostatic drug.

It penetrates tissues and stops the growth of tubercle bacillus.

Half life: half an hour.

123. Ethionamide

It is also bacteriostatic.

Mechanism of action: By inhibiting the cell wall synthesis.

124. Cycloserine

It also acts by inhibition of bacterial cell wall synthesis.

125.

Rifabutin

Rifapantin

Cepreomycin

Amikacin & kanamycin

Viomycin

Clofazimine

Macrolides

Thiacetazone

Quinolones:ciprofloxacin, levofloxacin, ofloxacin

126. Treatment for the Latent (inactive) TB infection.. 127. Dots: directly observed therapy short course..

(Six month regimen)

Rx

Rifampicin 600mg O.D.

Isoniazid 300mg given in combination 30minutes before breakfast

Pyridoxine 10 mg O.D.

128. Longer regimen

:

Isoniazid for 9 months daily or twice weekly OR Rifampin & pyrozinamide O.D. for 2 months. Mainly in isoniazid resistant TB. OR Rifampin O.D. for 4 months for one who cannot tolerate pyrazinamide. 129. For active TB

Most commonly used drugs are Isoniazid, rifampin and pyrazinamide daily for two months followed by isoniazid and rifampin B.D. or T.D. for 4 months.

If isoniazid resistance is suspected than ethmabutol or streptomycin.

In HIV patient: 9 to 10 months.

130. THANK YOU.....