Shree Ganeshaya namah
WELCOME WELCOME
RAJAYAKSHMA        TUBERCULOSIS
Shree Ganeshaya Namah…..
   A Seminar by: Sandeep kumar sharma    Guided by: Dr.Samir Bhadri    HOD in maulika siddanta    SDAC Siddapur (N.K.)
Dedicated to my  respected Father and  mother…..
Acc. to Ayurveda
Synonyms अनेक रोगानुगतो बहुरोगपुरोगम : दुर्विग्नेयो दुर्निवार :  शोषो महाबल :( सु . सं . उ . ४१ / ३ )
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.
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)
Due to occurrence of disease first time in Raja so called as Rajayakshma.
Hetu इह खलु चत्वारि शोषस्यायतनानि भवन्ति ; तधथा - साहसं ,  संधारणं क्षयो   विषमाशनमिति ( च . सं . नि .  6/3 ) (c.s.ni.6/3 and s.s.u.41/9)
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
क्षयाद्वेगप्रतीघातादाघाताद्विषमाशनात् जायते कुपितैर्दोषै : व्याप्तदेहस्य देहिन :( सु . सं . उ .  41/9 )
There are four etiological factors acc. To susruta Khsaya Vega pratighata Aaghata vishamaashana
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
- 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. .
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.
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.
Lakshanas These vitiated doshas after entering the sandhi’s (joints) cause: Jrambha (yawning),  Angamarda (Pain in body parts) and  Jwara (fever).
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)
After entering the Pranavaha srotasas causes: Swasa (dyspnoea) Pratishyaya (rhinitis) After entering in head produces: Sira shula (distress in head)
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
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)
Samprapti of    sandharana 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.
Lakshanas of sandharana janya    Rajayakshma 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
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)
All above etiological factors leads to Rasa dhatu kshaya which leads to manifestation of sosa Roga. Delay in management causes Rajayakshma.
Pratiloma kshayaja Hetu Ati Maithuna
- Ati Maithuna leads to Shukra    dhatu kshaya   - after Shukra kshaya if person   indulges in sexual activity   - no semen ejaculation   - vata enters the blood vessels    and causes blood discharge    having vata gunas from seminal   passage. Samprapti of kshaya janya Rajayakshma
vitiated vata spreading the entire body and aggravates Pitta and kapha Pitta dries up the mamsa and rakta  leads to sosa leads to Rajayakshma
Lakshanas Pain in the side of the chest and shoulders. irritation in throat Angamarda Aruchi Indigestion Jwara, kasa, swarabhada, pratishyaya (due to pratiloma vata)
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. That’s why one should protect his Shukra dhatu.
Vishamashana hetu If  the person adopts unhealthy dietetic pattern will lead to Rajayakshma.
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.
Here vitiated Vata leads to: Shula Angamarda Kanthodhwamsa Parshva samrujan swarabheda pratishyaya
Here vitiated Pitta leads to: Jwara Atisara Antardaha
Here vitiated kapha leads to: Pratishyaya Aruchi Kasa Siraso gurutvam
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.
Samprapti of Rajayakshma कफप्रधानैर्दोषैर्हि रुद्द्देषु रसवर्त्मसु अतिव्यवायिनो वा अपि क्षीणे रेतस्यनन्तरम् क्षीयन्ते धातव :  सर्वे तत :  शुष्यति मानव : ( सु . सं . उ .  41/9-10 )
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.
तैरुदीर्णो अनिल :  पित्तम् कफम् च उदीर्य सर्वत : शरीरसन्धीनाविश्य तान् सिराम् च प्रपीडयन् मुखानि स्रोतसाम् रुद्ध्वा तथैवातिविव्रत्य वा सर्पन्नूर्ध्वमधस्तिर्यग्यथास्वम् जनयेद् गदान् ( अ . ह्र . नि .  5/5-6 )
Samprapti  acc. 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.
Rajayakshma Samprapti ghatakas Dosa : kapha pradhana tridoshas Vata (vyana, samana, udana, prana and  apana) 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)
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.
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
Sadhya asadhyatva Sadhya in strong person Asadhya in weak person
पूर्वरुपं प्रतिश्यायो दौर्बल्यम् दोषदर्शनम् अदोषेष्वेपि भावेषु काये बीभत्सदर्शनम् घृणित्वमश्नतश्चापि बलमांसपरीक्षय : स्त्रीमद्यमांसप्रियता प्रियता चावगुण्ठने मक्षिकाघुणकेशानां तृनानां पतनानि च प्रायो अन्नपाने केशानां नखानां चाभिवर्धनम् पतत्रिभि :  पतंगै :  च श्वादैश्चाभिधर्पणम् स्वप्ने केशास्थिराशीनाम् भस्मनश्चाधिरोहनम् जलाशयानाम् शैलानां वनानां ज्योतिपामपि शुष्यतां क्षीयमाणानां पततां यच्च दर्शनम् प्राग्रूपं बहुरुपम्य तद्ग्येयं राजयक्ष्मण :( च . स . चि .8/33-36) पूर्वरूप
श्वास अंगमर्द कफसंस्रव तालुशोष वमि अग्निसाद मद पीनस कास निद्रा शोषे भविष्यति भवन्ति स चापि जन्तु :  शुक्लेक्षणो भवति मांसपरोरिरंसु : स्वप्नेषु काकशुक शल्ल्की नीलकण्ठा गृध्रास्तथैव कपय :  कृकलासकाश्च तं वाहयन्ति स नदीर्विजलाश्च पश्येत् शुष्कान् तरून् पवन धूमदवार्दितांश्च  ( सु . सं . उ .41)
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
Frequent looking at the hands Excessive whitishness of eyes Swasa Angamarda Talushosa Vamana Agninasha Mada Nidra
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.
त्रिरूप राजयक्ष्मा त्रिभिर्वा पीडितं लिंगै :  ज्वर कासासृगामयै : ( सु . सं . उ .41/15) jwara kasa haemoptysis
षड् रूप राजयक्ष्मा Acc. To charaka कासो संतापो वैस्वर्यं ज्वर :  पार्श्वशिरोरुजा : छर्दनं रक्तकफयो :  श्वासो वर्चोगदो अरुचि : रुपानि एकादशैतानि यक्ष्मण :  षडिमानि वा कासो ज्वर :  पार्श्वशूलं स्वरवर्चोगदो अरुचि : सर्वै :  अधै :  त्रिभि :  वा अपि लिंगै :  मांस बल क्षये युक्तो वर्ज्य : चिकित्स्यस्तु सर्वरुपो अपि अतो अन्यथा ( च . चि .8/45-47)
kasa santapa or fever vaiswarya ( derangement of voice) parshva shiro ruja diarrhoea Aruchi (anorexia)
षड् रूप राजयक्ष्मा   Acc. To susruta भक्तद्वेषो ज्वर :  श्वास :  कास :  शोणितदर्शनम् स्वरभेदश्च जायेत् षड् रूपं राजयक्ष्मणि  ( सु . स . उ .41/5)
bhakta dwesha jwara Swasa kasa rakta shtheevana swarabheda
एकादश रूपानि राजयक्ष्मा   Acc. To charaka अत् ऊर्ध्वम् एकादश रूपानि तस्य भवन्ति ,  तद्यथा -  शिरस :  परिपूर्णत्वम् ,  कास :,  श्वास :, स्वरभेद :,  श्लेष्मणश्छर्दनम् ,  शोणितष्ठीवनम् , पार्श्वसंरोजनम् ,  अंसावमर्द :,  ज्वर :,  अतिसार :,  अरोकश्चेति ( च . स . नि .6/14)
shiras paripurnatwam kasa Swasa swarabheda vomiting of shleshma shonita shtheevana (haemoptysis) parshva ruja ansavmarda jwara atisara arochaka
एकादश रूपानि राजयक्ष्मा   Acc. to susruta स्वरभेदो अनिलात् शूलं संकोच :  च अंसपार्श्वयो : ज्वरो दाहो अतिसारश्च पित्तात् रक्तस्य चागम : शिरस :  परिपूर्णत्वम् अभक्तच्छन्द एव च कास :  कंठस्य च उध्वंसो विग्गेय :  कफकोपत :( सु . स . उ .41/6-7)
Due to vata Swarabheda Amsha parshva sankocha Amsha parshva shula
Due to Pitta jwara daha atisara rakta shtheevana
Due to kapha heaviness of head Aruchi Kasa Kantha peeda
साध्य लक्षण s ज्वरानुबंधरहितं बलवन्तं क्रियासहम् उपक्रमेदात्मवन्तं दीप्ताग्निमकृशं   नरम् ( सु . स . उ .41/13) without fever balwaan kriyasahya deeptagni akrish
असाध्य लक्षण s   acc. to charaka दुर्बलम् तु अति क्षीण बल मांस शोणितम् अल्पलिंगमजातारिष्टमपि बहुलिंगमजातारिष्टमपि , बहुलिंगमजातारिष्टं च विद्यात् , असहत्वात् व्याधि औषध बलस्य ; तं परिवर्जयेत् , क्षणेनैव हि प्रादुर्भवन्ति अरिष्टानि अनिमित्तश्चारिष्ट प्रादुर्भाव इति ( च . स . नि .6/16)
Durbala Ati ksheena mamsa, bala and rakta Aushadha asahya
  acc. to susruta एकादशभिरेभिर्वा षड्भिर्वापि समन्वितम् कास अतीसार पार्श्वार्ति स्वर भेदारुचिज्वरै : त्रिभिर्वा पीडितं लिंगै : कासश्वासासृगामयै : जह्यात् शोषार्दितम् जन्तुमिच्छन् सुविमलम् यश : सर्वै :  अधै : त्रिभि वापि लिंगै :  मांसबलक्षये युक्तो वर्ज्य :  चिकित्स्यस्तु सर्वरूपो अपि अतो अन्यथा महाशनं क्षीयमानम् अतिसार निपीडितम् शूनमुष्कोदरं चैव यक्ष्मिणं परिवर्जयेत् शुक्लाक्षम् अन्न द्वेष्टारम् ऊर्ध्व श्वास निपीडतम् कृच्छ्रेण बहु मेहन्तं यक्ष्मा हन्ति इह   मानवम् ( सु . सं . उ .41/8-12)
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.
कारणानुसार शोषभेदान् व्यवायशोकवार्धक्यव्यायामाध्वप्रशोषितान् व्रणोर :  क्षतसंग्यौ च शोषिणौ लक्षणै :  श्रृणु  ( सु . स . उ .41/14)
vyavaya shoka vardhakya (vriddhavastha) vyaayama aadhva vrana urakshata
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.
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.
उपशय औषध : Sitopalaladi churna Durlabhadighrita Jivantyadighrita Talisadi churna and gutika
Acc. To modern science…..
TUBERCULOSIS Pulmonary
Some terms related to the topic Hilar - related to hilum or hilus. Lesions - discontinuation of tissues. primary focus- the  starting point of disease process. Tabes  Mesenterica  - a progressive wasting of the Intestine.
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.
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.
Droplet infection Droplet – very small drop. Spreading of infection by fine infected particles as by sneezing from the nose or by spitting from mouth.
Causative organism Tubercle bacillus or Koch’s bacillus or  Mycobacterium Tuberculosis. Organism  is a strict aerobe and lives in the part where the  oxygen supply  is more,   Like  apex of the lungs .  Mycobacterium Tuberculosis Bovis  is mainly a causative factor by the  unpasturated  milk from the animals.
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.  
Tuberculosis is an infectious disease caused by  Mycobacterium tuberculosis . The disease primarily affects lungs and causes  Pulmonary 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 as  Bovine Tuberculosis .
Atypical or non tuberculous mycobacteria   Atypical term is used for the other species of Mycobacteria rather than Mycobacterium tuberculosis complex also called as  environmental Mycobacteria.  
Mode of transmission   Human beings acquire infection with tubercle bacilli by following routes: 1)  Inhalation :  from cough droplets or dried sputum from an open case of  Pulmonary 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.
Incubation period   Development of disease depends upon the closeness of contact, extent of disease and  sputum positivity  of 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 .
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.
4)  By the natural passages :     (A) Lung lesions into pleura   (B) Transbronchial spread into adjacent lung segments (C) Into peritoneal cavity (tuberculous  peritonitis)   (D) Infected sputum into larynx ( Tuberculous laryngitis )   (E) Swallowing of infected sputum ( illeocaecal tuberculosis ) (F) Renal lesions into ureter
Evolution  of tubercle   Tubercle bacilli invasion lodges in pulmonary capillaries due to tubercle bacilli coating of  opsonin  with in 12 hours progressive infiltration by macrophages occurs phagocytosis by macrophages activation of T&B lymphocyte cells B cells produce antibodies but don’t have any role in defence against tubercle bacillus T helper cell(CD4+T) inactivation
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.
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
Primary TB   The infection of an indivisual who has not been previously infected or immunised is called  Primary TB  or  Ghon’s complex  or  childhood 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.
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.
Note : In the case of Primary TB of the alimentary tract due to ingestion of tubercle bacilli a small  primary focus  (the starting point of disease process) is seen in intestine with enlarged lymph nodes producing  Tabes Mesentrica  (a progressive wasting of the Intestine). The enlarged and Caseous mesenteric lymph nodes may rupture into peritoneal cavity and may cause  tuberculous peritonitis.
Fate of Primary TB   1) The lesions of lung may not progress but instead of healing by  fibrosis, calcification  and  ossification  may occur. 2) Primary focus continues to grow and Caseous material is sent to the other part of the same lung or to another lung. It is called as  Progressive primary TB. 3) Bacilli may enter the circulation through  erosion ( destruction of tissue) in blood vessels and may spread to various tissues and organs. This is called  Primary milliary TB. 4) Healed lesions of primary TB may be reactivated. It is called  Progressive secondary TB.
Secondary Tuberculosis   Infection of an 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.
Secondary TB occurs mainly in apex of the lungs. Other sites of infection are tonsils, pharynx, larynx, small intestine and skin.
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
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 TB  is more common in HIV patients.
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:
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.
Systemic features   Fever Night sweating Fatigue Loss of weight and appetite Note:  Untreated cases may develop  systemic secondary amyloidosis .
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 as  tuberculin units(TU). For routine testing - 1 TU  dose is used.
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.
1. Mantoux test   It is carried out by injecting 1 TU of PPD in 0.1 ml on the flexor surface of forearm intradermally. WHO advocates  “PPD-RT-23 with tween 80”  preparation for testing. Result is read out after 72 hours of injection by seeing the diameter of induration.
If the diameter is more than 10mm then  Positive case tests . If the diameter is less than 6mm then  negative case test. If the diameter is in b/w 6 to 10 mm then doubtful case test.
2. Positive sputum for AFB (on smear or culture) 3. complete haemogram ( lymphocytosis ) 4. Chest X-RAY 5. Fibreoptic bronchoscopy 6. Biopsy
Causes of death in Pulmonary TB   Pulmonary insufficiency  Pulmonary haemorrhages Sepsis (presence of micro organism in blood) Cor pulmonate or  secondary Amyloidosis .
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
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.
Treatment   Treatment given in TB is called as  chemotherapy , which is having drugs of: highly effective  free from side effects  easy to administer  reasonably cheap
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.
The three basic concepts in 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.
Antituberculous drugs  are classified as…..
First  line antituberculosis drugs   Superior in efficacy and posses an acceptable degree of toxicity. these are:  Isoniazid, rifampin, pyrazinamide, ethmabutol, streptomycin.
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.
Rifampin   Mechanism of action: It inhibits the DNA synthesis no further growth of tubercle bacilli.
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.
Ethamabutol   It also inhibits the DNA synthesis.  Half life: 3 to 4 hours.
Streptomycin   Bactericidal.
Second line antituberculosis drugs …..
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.
Para-aminosalicylic acid (PAS)   It is a Bacteriostatic drug. It penetrates tissues and stops the growth of tubercle bacillus. Half life: half an hour.
Ethionamide   It is also bacteriostatic. Mechanism of action: By inhibiting the cell wall synthesis.
Cycloserine   It also acts by inhibition of bacterial cell wall synthesis.
Rifabutin   Rifapantin   Cepreomycin   Amikacin & kanamycin   Viomycin   Clofazimine   Macrolides   Thiacetazone   Quinolones:  ciprofloxacin, levofloxacin, ofloxacin
Treatment for the  Latent (inactive) TB infection…..
Dots: directly observed therapy short course….. (Six month regimen) Rx   Rifampicin 600mg O.D.   Isoniazid 300mg given in combination 30  minutes before breakfast Pyridoxine 10 mg O.D.
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.  
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. I f isoniazid resistance is suspected than ethmabutol or streptomycin. In HIV patient: 9 to 10 months.
THANK YOU.....

Rajayakshma or Tuberculosis by Dr.Sandeep sharma

  • 1.
  • 2.
  • 3.
    RAJAYAKSHMA      TUBERCULOSIS
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  • 5.
      ASeminar 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.
  • 8.
    Synonyms अनेक रोगानुगतोबहुरोगपुरोगम : दुर्विग्नेयो दुर्निवार : शोषो महाबल :( सु . सं . उ . ४१ / ३ )
  • 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 married28 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 occurrenceof disease first time in Raja so called as Rajayakshma.
  • 12.
    Hetu इह खलुचत्वारि शोषस्यायतनानि भवन्ति ; तधथा - साहसं , संधारणं क्षयो विषमाशनमिति ( च . सं . नि . 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
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  • 15.
    There are fouretiological factors acc. To susruta Khsaya Vega pratighata Aaghata vishamaashana
  • 16.
    When a persondoes 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 aweek 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 aresult 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 injuryto 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 vitiateddoshas after entering the sandhi’s (joints) cause: Jrambha (yawning), Angamarda (Pain in body parts) and Jwara (fever).
  • 21.
    After entering theAmashaya 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 thePranavaha srotasas causes: Swasa (dyspnoea) Pratishyaya (rhinitis) After entering in head produces: Sira shula (distress in head)
  • 23.
    2) Sandharanajaor 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 ofgentleman 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 of sandharana 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 sandharanajanya Rajayakshma 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 etiologicalfactors leads to Rasa dhatu kshaya which leads to manifestation of sosa Roga. Delay in management causes Rajayakshma.
  • 29.
  • 30.
    - Ati Maithunaleads to Shukra dhatu kshaya - after Shukra kshaya if person indulges in sexual activity - no semen ejaculation - vata enters the blood vessels and causes blood discharge having vata gunas from seminal passage. Samprapti of kshaya janya Rajayakshma
  • 31.
    vitiated vata spreadingthe entire body and aggravates Pitta and kapha Pitta dries up the mamsa and rakta leads to sosa leads to Rajayakshma
  • 32.
    Lakshanas Pain inthe side of the chest and shoulders. irritation in throat Angamarda Aruchi Indigestion Jwara, kasa, swarabhada, pratishyaya (due to pratiloma vata)
  • 33.
    Excess kasa leadsto sputum along with rakta and due to rakta kshaya further dhatu formation stops and person becomes weekend and leads to Rajayakshma. That’s why one should protect his Shukra dhatu.
  • 34.
    Vishamashana hetu If the person adopts unhealthy dietetic pattern will lead to Rajayakshma.
  • 35.
    Samprapti of vishamashanajaRajayakshma 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 Vataleads to: Shula Angamarda Kanthodhwamsa Parshva samrujan swarabheda pratishyaya
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    Here vitiated Pittaleads to: Jwara Atisara Antardaha
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    Here vitiated kaphaleads to: Pratishyaya Aruchi Kasa Siraso gurutvam
  • 39.
    In this caseone 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 Rajayakshmaकफप्रधानैर्दोषैर्हि रुद्द्देषु रसवर्त्मसु अतिव्यवायिनो वा अपि क्षीणे रेतस्यनन्तरम् क्षीयन्ते धातव : सर्वे तत : शुष्यति मानव : ( सु . सं . उ . 41/9-10 )
  • 41.
    Samprapti: Acc. Tosusruta 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.
    तैरुदीर्णो अनिल : पित्तम् कफम् च उदीर्य सर्वत : शरीरसन्धीनाविश्य तान् सिराम् च प्रपीडयन् मुखानि स्रोतसाम् रुद्ध्वा तथैवातिविव्रत्य वा सर्पन्नूर्ध्वमधस्तिर्यग्यथास्वम् जनयेद् गदान् ( अ . ह्र . नि . 5/5-6 )
  • 43.
    Samprapti acc.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 ghatakasDosa : kapha pradhana tridoshas Vata (vyana, samana, udana, prana and apana) 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 : sanghaand 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 Sadhyain strong person Asadhya in weak person
  • 48.
    पूर्वरुपं प्रतिश्यायो दौर्बल्यम्दोषदर्शनम् अदोषेष्वेपि भावेषु काये बीभत्सदर्शनम् घृणित्वमश्नतश्चापि बलमांसपरीक्षय : स्त्रीमद्यमांसप्रियता प्रियता चावगुण्ठने मक्षिकाघुणकेशानां तृनानां पतनानि च प्रायो अन्नपाने केशानां नखानां चाभिवर्धनम् पतत्रिभि : पतंगै : च श्वादैश्चाभिधर्पणम् स्वप्ने केशास्थिराशीनाम् भस्मनश्चाधिरोहनम् जलाशयानाम् शैलानां वनानां ज्योतिपामपि शुष्यतां क्षीयमाणानां पततां यच्च दर्शनम् प्राग्रूपं बहुरुपम्य तद्ग्येयं राजयक्ष्मण :( च . स . चि .8/33-36) पूर्वरूप
  • 49.
    श्वास अंगमर्द कफसंस्रवतालुशोष वमि अग्निसाद मद पीनस कास निद्रा शोषे भविष्यति भवन्ति स चापि जन्तु : शुक्लेक्षणो भवति मांसपरोरिरंसु : स्वप्नेषु काकशुक शल्ल्की नीलकण्ठा गृध्रास्तथैव कपय : कृकलासकाश्च तं वाहयन्ति स नदीर्विजलाश्च पश्येत् शुष्कान् तरून् पवन धूमदवार्दितांश्च ( सु . सं . उ .41)
  • 50.
    Purvarupas Pratishyaya DorbalyaStree 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 atthe hands Excessive whitishness of eyes Swasa Angamarda Talushosa Vamana Agninasha Mada Nidra
  • 52.
    In dreams hesees: Empty reservoirs deserted villages, towns, cities and countries dried, burnt, and destroyed forest. Riding over dog, camel, donkey and pig etc.
  • 53.
    त्रिरूप राजयक्ष्मा त्रिभिर्वापीडितं लिंगै : ज्वर कासासृगामयै : ( सु . सं . उ .41/15) jwara kasa haemoptysis
  • 54.
    षड् रूप राजयक्ष्माAcc. To charaka कासो संतापो वैस्वर्यं ज्वर : पार्श्वशिरोरुजा : छर्दनं रक्तकफयो : श्वासो वर्चोगदो अरुचि : रुपानि एकादशैतानि यक्ष्मण : षडिमानि वा कासो ज्वर : पार्श्वशूलं स्वरवर्चोगदो अरुचि : सर्वै : अधै : त्रिभि : वा अपि लिंगै : मांस बल क्षये युक्तो वर्ज्य : चिकित्स्यस्तु सर्वरुपो अपि अतो अन्यथा ( च . चि .8/45-47)
  • 55.
    kasa santapa orfever vaiswarya ( derangement of voice) parshva shiro ruja diarrhoea Aruchi (anorexia)
  • 56.
    षड् रूप राजयक्ष्मा Acc. To susruta भक्तद्वेषो ज्वर : श्वास : कास : शोणितदर्शनम् स्वरभेदश्च जायेत् षड् रूपं राजयक्ष्मणि ( सु . स . उ .41/5)
  • 57.
    bhakta dwesha jwaraSwasa kasa rakta shtheevana swarabheda
  • 58.
    एकादश रूपानि राजयक्ष्मा Acc. To charaka अत् ऊर्ध्वम् एकादश रूपानि तस्य भवन्ति , तद्यथा - शिरस : परिपूर्णत्वम् , कास :, श्वास :, स्वरभेद :, श्लेष्मणश्छर्दनम् , शोणितष्ठीवनम् , पार्श्वसंरोजनम् , अंसावमर्द :, ज्वर :, अतिसार :, अरोकश्चेति ( च . स . नि .6/14)
  • 59.
    shiras paripurnatwam kasaSwasa swarabheda vomiting of shleshma shonita shtheevana (haemoptysis) parshva ruja ansavmarda jwara atisara arochaka
  • 60.
    एकादश रूपानि राजयक्ष्मा Acc. to susruta स्वरभेदो अनिलात् शूलं संकोच : च अंसपार्श्वयो : ज्वरो दाहो अतिसारश्च पित्तात् रक्तस्य चागम : शिरस : परिपूर्णत्वम् अभक्तच्छन्द एव च कास : कंठस्य च उध्वंसो विग्गेय : कफकोपत :( सु . स . उ .41/6-7)
  • 61.
    Due to vataSwarabheda Amsha parshva sankocha Amsha parshva shula
  • 62.
    Due to Pittajwara daha atisara rakta shtheevana
  • 63.
    Due to kaphaheaviness of head Aruchi Kasa Kantha peeda
  • 64.
    साध्य लक्षण sज्वरानुबंधरहितं बलवन्तं क्रियासहम् उपक्रमेदात्मवन्तं दीप्ताग्निमकृशं नरम् ( सु . स . उ .41/13) without fever balwaan kriyasahya deeptagni akrish
  • 65.
    असाध्य लक्षण s acc. to charaka दुर्बलम् तु अति क्षीण बल मांस शोणितम् अल्पलिंगमजातारिष्टमपि बहुलिंगमजातारिष्टमपि , बहुलिंगमजातारिष्टं च विद्यात् , असहत्वात् व्याधि औषध बलस्य ; तं परिवर्जयेत् , क्षणेनैव हि प्रादुर्भवन्ति अरिष्टानि अनिमित्तश्चारिष्ट प्रादुर्भाव इति ( च . स . नि .6/16)
  • 66.
    Durbala Ati ksheenamamsa, bala and rakta Aushadha asahya
  • 67.
    acc.to susruta एकादशभिरेभिर्वा षड्भिर्वापि समन्वितम् कास अतीसार पार्श्वार्ति स्वर भेदारुचिज्वरै : त्रिभिर्वा पीडितं लिंगै : कासश्वासासृगामयै : जह्यात् शोषार्दितम् जन्तुमिच्छन् सुविमलम् यश : सर्वै : अधै : त्रिभि वापि लिंगै : मांसबलक्षये युक्तो वर्ज्य : चिकित्स्यस्तु सर्वरूपो अपि अतो अन्यथा महाशनं क्षीयमानम् अतिसार निपीडितम् शूनमुष्कोदरं चैव यक्ष्मिणं परिवर्जयेत् शुक्लाक्षम् अन्न द्वेष्टारम् ऊर्ध्व श्वास निपीडतम् कृच्छ्रेण बहु मेहन्तं यक्ष्मा हन्ति इह मानवम् ( सु . सं . उ .41/8-12)
  • 68.
    One who ishaving 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.
    कारणानुसार शोषभेदान् व्यवायशोकवार्धक्यव्यायामाध्वप्रशोषितान्व्रणोर : क्षतसंग्यौ च शोषिणौ लक्षणै : श्रृणु ( सु . स . उ .41/14)
  • 70.
    vyavaya shoka vardhakya(vriddhavastha) vyaayama aadhva vrana urakshata
  • 71.
    Difference between sosaand 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 becalled 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.
    उपशय औषध :Sitopalaladi churna Durlabhadighrita Jivantyadighrita Talisadi churna and gutika
  • 74.
    Acc. To modernscience…..
  • 75.
  • 76.
    Some terms relatedto the topic Hilar - related to hilum or hilus. Lesions - discontinuation of tissues. primary focus- the starting point of disease process. Tabes  Mesenterica - a progressive wasting of the Intestine.
  • 77.
    Caseous - cheesyappearance 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 isdisease 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 Tuberclebacillus or Koch’s bacillus or Mycobacterium Tuberculosis. Organism is a strict aerobe and lives in the part where the oxygen supply is more,   Like apex of the lungs . Mycobacterium Tuberculosis Bovis is mainly a causative factor by the unpasturated milk 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 aninfectious disease caused by Mycobacterium tuberculosis . The disease primarily affects lungs and causes Pulmonary 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 as Bovine Tuberculosis .
  • 83.
    Atypical or nontuberculous mycobacteria Atypical term is used for the other species of Mycobacteria rather than Mycobacterium tuberculosis complex also called as environmental Mycobacteria.  
  • 84.
    Mode of transmission Human beings acquire infection with tubercle bacilli by following routes: 1) Inhalation : from cough droplets or dried sputum from an open case of Pulmonary 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 and sputum positivity of 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) Bythe natural passages :   (A) Lung lesions into pleura   (B) Transbronchial spread into adjacent lung segments (C) Into peritoneal cavity (tuberculous peritonitis)   (D) Infected sputum into larynx ( Tuberculous laryngitis )   (E) Swallowing of infected sputum ( illeocaecal tuberculosis ) (F) Renal lesions into ureter
  • 88.
    Evolution oftubercle Tubercle bacilli invasion lodges in pulmonary capillaries due to tubercle bacilli coating of opsonin with in 12 hours progressive infiltration by macrophages occurs phagocytosis by macrophages activation of T&B lymphocyte cells B cells produce antibodies but don’t have any role in defence against tubercle bacillus T helper cell(CD4+T) inactivation
  • 89.
    without T helpercell 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 called Primary TB or Ghon’s complex or childhood 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 ofTB 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 : Inthe case of Primary TB of the alimentary tract due to ingestion of tubercle bacilli a small primary focus (the starting point of disease process) is seen in intestine with enlarged lymph nodes producing Tabes Mesentrica (a progressive wasting of the Intestine). The enlarged and Caseous mesenteric lymph nodes may rupture into peritoneal cavity and may cause tuberculous peritonitis.
  • 94.
    Fate of PrimaryTB 1) The lesions of lung may not progress but instead of healing by fibrosis, calcification and ossification may occur. 2) Primary focus continues to grow and Caseous material is sent to the other part of the same lung or to another lung. It is called as Progressive primary TB. 3) Bacilli may enter the circulation through erosion ( destruction of tissue) in blood vessels and may spread to various tissues and organs. This is called Primary milliary TB. 4) Healed lesions of primary TB may be reactivated. It is called Progressive secondary TB.
  • 95.
    Secondary Tuberculosis Infection of an 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 occursmainly 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 TB is more common in HIV 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 develop systemic 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 as tuberculin units(TU). For routine testing - 1 TU dose is used.
  • 103.
    Milliary TB Thisdisease 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 injecting 1 TU of PPD in 0.1 ml on the flexor surface of forearm intradermally. WHO advocates “PPD-RT-23 with tween 80” preparation for testing. Result is read out after 72 hours of injection by seeing the diameter of induration.
  • 105.
    If the diameteris more than 10mm then Positive case tests . If the diameter is less than 6mm then negative case test. If the diameter is in b/w 6 to 10 mm then doubtful case test.
  • 106.
    2. Positive sputumfor AFB (on smear or culture) 3. complete haemogram ( lymphocytosis ) 4. Chest X-RAY 5. Fibreoptic bronchoscopy 6. Biopsy
  • 107.
    Causes of deathin Pulmonary TB Pulmonary insufficiency Pulmonary haemorrhages Sepsis (presence of micro organism in blood) Cor pulmonate or secondary 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 as chemotherapy , which is having drugs of: highly effective free from side effects easy to administer reasonably cheap
  • 111.
    Currently used drugsmay 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 basicconcepts in 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 drugs are classified as…..
  • 114.
    First lineantituberculosis drugs Superior in efficacy and posses an acceptable degree of toxicity. these are: Isoniazid, rifampin, pyrazinamide, ethmabutol, streptomycin.
  • 115.
    Isoniazid Mechanism ofaction: 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.
  • 121.
    Second line antituberculosisdrugs 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 observedtherapy short course….. (Six month regimen) Rx Rifampicin 600mg O.D. Isoniazid 300mg given in combination 30 minutes 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. I f isoniazid resistance is suspected than ethmabutol or streptomycin. In HIV patient: 9 to 10 months.
  • 130.