Synonyms
अनेक रोगानुगतो बह
ुरोगपुरोगम
:
दि
ुिगि नेयो दिुनिि ार
: 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 चतिािर शोषसयायतनािन भििित;
तधथा-साहसं, संधारणं कयो
ििषमाशनिमित(च.सं.िन. 6/3)
(c.s.ni.6/3 and s.s.u.41/9)(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
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 aaghataja1.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
•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 janyaSamprapti of kshaya janya
RajayakshmaRajayakshma
•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 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:
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.
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
पूिरि पं पितशयायो दौबलि यम
्दोषदशनि म्
अदोषेषिेिप भािेषु काये बीभतसदशनि म
्
घिृणतिमशतशािप बलमांसपरीकय:
सीमदमांसिपयता िपयता चािगुणठने
मिककाघुणकेशानां तनृ ानां पतनािन च
पायो अिनपाने केशानां नखानां चािभिधनि म
्
पतिििभ: पतंगै: च शादैशािभधपणि म
्
सिपने केशािसथराशीनाम
्भसमनशािधरोहनम्
जलाशयानाम
्शैलानां िनानां जयोितपामिप
शुषयतां कीयमाणानां पततां यचच दशनि म
्
पागूपं बह
ुरपमय तदगयेयं राजयकमण
:(च.स.िच.8/33-36)
पूििरप
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.
•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.
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.
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.
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.