A CLINICAL STUDY ON

DIAGNOSTIC METHDOLOGY OF PAANDU

- THROUGH SIDDHA PARAMETERS

Dissertation submitted To
THE TAMIL NADU DR.M.G.R. MEDICAL UNIVERSITY,

Chennai – 32.

For the partial fulfillment in Awarding the Degree of

DOCTOR OF MEDICINE (SIDDHA)

(Branch V – PG NOI NAADAL)

DEPARTMENT OF NOI NAADAL

GOVERNMENT SIDDHA MEDICAL COLLEGE
PALAYAMKOTTAI – 627002.
OCTOBER 2019
 GOVERNMENT SIDDHA MEDICAL COLLEGE AND HOSPITAL,
PALAYAMKOTTAI, THIRUNELVELI – 627002,
TAMILNADU, INDIA.

PHONE NO – 0462-2572736/2572737/2582010 FAX – 0462582010

DECLARATION BY THE CANDIDATE

I hereby declare that this dissertation entitled “A CLINICAL

STUDY ON DIAGNOSTIC METHODOLOGY OF PAANDU
(ANAEMIA) - THROUGH SIDDHA PARAMETERS” is a bonafide
and genuine research work carried out by me under the Guidance and
supervision of Prof. R. Neelavathy MD(S), Ph.D, Principal, Government
Siddha Medical College and Hospital, Palyamkottai, Thirunelveli, Tamil
Nadu, India. and the dissertation has not formed the basis for the award of
any Degree, Diploma, Fellowship or other similar title.

Date: Signature of the Candidate

Place: PALAYAMKOTTAI ( DR.MURUGAMOORTHY THUSIYANTHAN)

GOVERNMENT SIDDHA MEDICAL COLLEGE AND HOSPITAL,
PALAYAMKOTTAI, THIRUNELVELI – 627002,
TAMILNADU, INDIA.

PHONE NO – 0462-2572736/2572737/2582010 FAX – 0462582010

CERTIFICATE

Certify that I have gone through the dissertation submitted by

DR. MURUGAMOORTHY THUSIYANTHAN (Reg No – 321615008)
with the title,“ A CLINICAL STUDY ON DIAGNOSTIC
METHODOLOGY OF PAANDU (ANAEMIA) - THROUGH SIDDHA
PARAMETERS” , the student of final DOCTOR OF MEDICINE
(SIDDHA), Department of Noi Naadal (Branch –V) of the
GOVERNMENT SIDDHA MEDICAL COLLEGE AND HOSPITAL,
PALAYAMKOTTAI, TAMIL NADU, INDIA. This dissertation does not
represent or reproduce the dissertatin submitted and approved earlier.

Date:

Place : Palayamkottai HEAD OF THE DEPARTMENT

DEPARTMENT OF NOI NAADAL
 GOVERNMENT SIDDHA MEDICAL COLLEGE AND HOSPITAL,
PALAYAMKOTTAI, THIRUNELVELI – 627002,
TAMILNADU, INDIA.
PHONE NO – 0462-2572736/2572737/2582010 FAX – 0462582010

BONAFIDE CERTIFICATE
This is to certify that the dissertation entitled “ A CLINICAL STUDY ON
DIAGNOSTIC METHODOLOGY OF PAANDU (ANAEMIA)-
THROUGH SIDDHA PARAMETERS” is a bonafide work done by DR.
MURUGAMOORTHY THUSIYANTHAN (Reg No –321615008),
GOVERNMENT SIDDHA MEDICAL COLLEGE AND HOSPITAL,
PALAYAMKOTTAI in a partial fulfillment of the university rules and
regulations for award for MD (S) NOINAADAL under my guidance and
supervision during the academic year 2016 – 2019.
Name and Signature of Guide :

Name and Signature of Head Of the Department :

Name and Signature of Principal :

 ACKNOWLEDGEMENT

First and foremost, I thank the “ Almighty God” who’s always been
as strength wisdom and guides throughout the process of bringing out my
Dissertation work successfully.
I would like to extend my thanks to Siddhars, because of their
blessing to complete this work.
I heartfelt thanks my Parents and family members for giving me
this opportunity and the blessings to fulfill this work.

I express my sincere thanks to the Secretary, Ministry of AYUSH,

Health & Family Welfare, New Delhi.

I take this opportunity to express my gratitude and acknowledge the

Vice Chanceller, The Tamil Nadu Dr. M.G.R. Medical University,
Chennai for permitting me to do this study.
I express my sincere thanks to Prof. Dr.R.Neelavathy , M.D(S),
PhD, Principal, Government Siddha Medical College and Hospital,
Palayamkottai for her valuable suggestions and effective guidance and
constant encouragement in completing my dissertation work. I am grateful to
her for holding me to a high research standard and enforcing strict validations
for each research result, and thus teaching me how to do research.
I would like to express my sincere thanks to Dr.S. Victoria M.D(S),
Vice Principal and Head of the Department of PG Noi Naadal, Government
Siddhs Medical College and Hospital, Palayamkottai for their
encouragement and valuable guidance throughout my entire study.
I would like to express my sincere thanks to Dr.S.Sundararajan
M.D(S), Lecturer Grade - I, Department of Noi Naadal, Government Siddhs
Medical College and Hospital, Palayamkottai for their encouragement of my
study. Excelled care, continuous support and optimistic approach, which
influenced me to accomplish this work successfully.
I express my sincere thanks to Prof. Dr. B.Malarvizhi M.D(S), Head
Of the Department, Department of Siddha maruththuva adippadai
thaththuvam, Government Siddha Medical College and Hospital,
Palayamkottai for their encouragement study.
I would like to express my sincere thanks to Dr.A. Balamurugan
M.D(S), Lecturer Grade - II, Department of Noi Naadal, Government Siddha
Medical College and Hospital, Palayamkottai for their encouragement of my
study.
I would like to express my sincere thanks to Dr.R.Meenakshi
Sundaram M.D(S), Lecturer Grade - II, Department of Udal Thaththuvam,
Government Siddhs Medical College and Hospital, Palayamkottai, for their
guidance .
I would like to express my heartfelt thanks to Dr. M.
Muththukkumaran, MD(S) Lecturer Grade II, Department of Noi Naadal,
Dr.M.Sankara Rama Subramanian M.D(S), Assistant Lecturer,
Department of Noi Naadal, Dr. B. Senthil Selvi MD(S), Assistant Lecturer,
Department of Noi Naadal, Prof. Dr.M. Krishnaveni, MD(S), PhD, Dr. J.
Sriram MD(S), Lecturer, Government Siddha Medical College and Hospital,
Palayamkottai for their encouragement of my study.
I express my sincere thanks to Prof. Dr. K. Swaminathan
MD(Pathology), Department of Pathology ,Govt .Medical College and
Hospital, Palayamkottai, for guidance, Suggestion and hopeful valuable
support in my study.
 I express my sincere thanks to Laboratory Staffs, Government Siddha
Medical College and Hospital, Palayamkottai for hopeful valuable support
in my study.
I express my sincere thanks to Staffs, Annai clinical Laboratory ,
Palayamkottai for valuable Laboratory support in my study.
I thank the library librarian Mrs.T.Poongodi MSc (Lib.Science) and
other library attendant of Government Siddha Medical College and Hospital,
Palayamkottai, from where I derived much of the literary support.
I heartfelt thanks my siththy Mrs.S.Balarani BA,PGDE,MEd,
PGDEM, Principal, J/Vadamaradchi Girls College, Jaffna, Srilanka for her
timely help during study.
I also thank all my friends, brothers and sisters for their help in this
dissertation.
Besides this, several people have knowingly and unknowingly helped
me in the successful completion of this project.
Last but not least, I would like to pay high regards to my wife work
Dr.Thusiyanthan Kalaichelvi MD(S), Department of Nanju Noolum
Maruthuva Neethi Noolum, Government Siddha Medical College and hospital,
Palayamkottai for their sincere encouragement throughout my research work.
S.NO CONTENTS PAGE NO
DECLARATION BY THE CANDIDATES i
CERTIFICATE BY HEAD OF THE DEPARTMENT ii
BONAFIDE CERTIFICATE iii
SCREENING COMMITTEE FOR TITLE SELECTION iv
CERTIFICATE OF APPROVAL v
ACKNOWLEDGEMENT vi
1. INTRODUCTION 1
2. AIM AND OBJECTIVES 4
3. ELUCIDATION OF DISSERTATION TOPIC PAANDU 5
4. REVIEW OF LITERATURES 7
4.1. SIDDHA ASPECTS 7
4.2. MODERN ASPECT 54
5. EVALUATION OF DISSERTATION TOPIC PAANDU 95
5.1. MATERIAL AND METHOD 95
5.2. DIAGNOSTIC METHODOLOGY 97
5.3. OBSERVATION AND RESULTS 99
6. DISCUSSION 144
7. SUMMARY 153
8. CONCLUSION 160
9. SIDDHA TREATMENT OF ANAEMIA 164
10. DIETARY REGIMEN 166
11. BIBILIOGRAPHY 169
10. ANNEXURES – I
a. PROFORMA
b. CONSENT FORM
c. RESEARCH METHODOLOGY CERTIFICATE
d. CME CERTIFICATE - 02
e. JOURNAL CERTIFICATE - 02
INTRODUCTION
Siddha system is an ancient medical practice mainly practiced in South
India, North and East part of Srilanka and Malasia. Siddha diagnosis is based on
examination of signs and symptoms and its correlation with environment and
timeline. This system states that the human body is made up of vatham, piththam
and kapham. These three are part of the environment and formed by the
combination of the five basic elements. Vatham is formed by combination of air
and space. This is construclive force. Piththam is formed by fire. This is the force
of preservation. Kapham is formed by earth and water. This is the destructive
force. In healthy state, these humors are in the ratio of 1(one), ½(half), ¼(quarter)
in equilibrium. They are called the life forces or humours and are explained in
pathinensiddhanaadi sasthiram. 1

“toq;fpa thjk; khj;jpiu nahd;whfpy;

joq;fpa gpj;jk; jd;dp yiu thrp

moq;Fq; fge; jhdlq;fpNa fhNyhby;

2
gpwq;fpNa rPtHf;Fg; gpr nfhd;Wkpy;iyNa”

Siddha diagnosis is unique in individualization with respect to locate the

vitiation of three humours of an individual’s constitution and not generalized 3,4,5,6.
Sage Yugi classified diseases mainly based on signs, symptoms and three
humours. This system of diagnosis tells about the prognosis of the condition too.
In the classical Siddha scripts different diagnostic procedures and symptoms of
the various diseases are mentioned.

The procedure of Neikuri (spreading pattern of oil on urine) and the

interpretation of the out comes are clearly mentioned by Agasthiar and Theraiyar.
7,
Envagai thervukal ( Eight fold Examination), a kind of systemic examination
include examining the Nadi ( Pulsation), Na (Tongue), Niram ( complexion),
Mozhi (Voice), Vizhi (Eye), Sparisam (Examination of body temperature and
touch sensation), Malam (Stool), and Mooththiram ( Urine). The present study
will planned to validate the diagnostic procedures of siddha system to diagnose
Paandu with aid on conventional clinical diagnostic procedures.

1
 Paandu (Anaemia is a disease with known diagnosis and prognosis will be
selected for the study. Siddha science has placed Anaemia not as a state or
condition but a disease. In Siddha, the term Paandu may be used instead of
Anaemia, Paandu is otherwise called Velluppunoi, Venpandu, etc. In this disease
the body, conjunctiva, nail bed, oral mucosa etc, appears pallor. There are six type
of paandu. Three are caused due to derangement of a specific humour Vatham or
Pitha or Kapham. One of the classifications is caused due to derangement of the
three humours together known as the Mukkutrap paandu. Another one type is
caused due to toxic manifestation in blood known as Nanju Paandu. This type is
incurable one. The last one is cause………………8
According to Agasthiar Gunavahadam stated about Paandu is,

“ ghulh ghz;Ltif nrhy;yf; Nfsha;

gupthd ghz;Lj jhdQ;Nr ahFk;

thulh thj gpj;jk; rPj ghz;L

tifahd tplghz;L kpUj;jpfh ghz;L

Njulh Njfj;jpy; ,uj;jk; tw;wpj;

jPq;fhd tpe;jNeha; fhZkg;gh

$wlh nrhy;YfpNwd; ed;wha;g; ghU

Fwpg;GlNd ePaijj; jhdwpe;Jnfhs;Ns 9

( mf];jpaH Fzthflk;)

In the script of Siddha the disease is the result of increased Pitham. The following
procedures, taken for the study namely Neikkuri, Eight fold examinations and
Manikkadai Nool (wrist circummetric sign) will be considered for this study. The
treatment in traditional system will be more valid if the disease is diagnosed by
its own perspective. So the present study will be carried out to validate the Siddha
diagnostic procedure for Paandu.

Paandu according to Siddha concept is caused by disturbances of blood

which is one of the Sapthadhathu (seven bodily tissues in our body). It is
Correlation of Paandu with types of anemia in modern science such as peripheral
smear, Blood grouping.
2
 Each and every developing country has it’s own problem of increasing
population, illiteracy, lack of awareness about public health and basic
environment knowledge etc.

India and Srilanka, because of poverty, socio- economic patterns,

illiteracy, malnutrition, untreated illness, hook- worm infestation are the common
cause of affliction of the disease “Paandu noi”, among the vast species of
population.

A large numbers of patients especially women and children are seen with
pale look and shining appearance, which are some land marks of under
nourishment Siddha system defines this condition as “Paandu noi” or “Veluppu
noi”.

Iron Deficiency is a common problem in women, children and elderly

people. In women, it is mainly due to menstrual problem and malnutrition. In
elders, it is mainly due to malnutrition. In children, it is mainly due to worm
infestation and malnutrition.

So, around the world malnutrition and blood loss are the most common
cause for iron and B12 deficiency anaemia.

3
 AIM AND OBJECTIVES

AIM

A clinical study on documentation of siddha diagnostic methodology for

PAANDU

OBJECTIVE

 Primary Objectives

1. To validate and document the Neerkuri and Neikuri in diagnosis of PAANDU

 Secondary Objectives

1. Validate and document the NAADI NADAI in diagnosis of PAANDU

2. To validate and document the MANIKKADAI NOOL in diagnosis of PAANDU

3. To correlation of Paandu with types of anaemia in modern science.

4
 ELUCIDATION OF DISSERTATION TOPIC PAANDU
“ ghulh ghz;Ltif nrhy;yf; Nfsha;

gupthd ghz;Lj jhdQ;Nr ahFk;

thulh thj gpj;jk; rPj ghz;L

tifahd tplghz;L kpUj;jpfh ghz;L

Njulh Njfj;jpy; ,uj;jk; tw;wpj;

jPq;fhd tpe;jNeha; fhZkg;gh

$wlh nrhy;YfpNwd; ed;wha;g; ghU

Fwpg;GlNd ePaijj; jhdwpe;Jnfhs;Ns” 9

( mf];jpaH Fzthflk;)

ghz;L Nehapd; tiffs;

1. thjg;ghz;L
2. gpj;jg; ghz;L
3. rPjg;; ghz;L
4. tplghz;L
5. kpUj;jpfh ghz;L
Mfpa Ie;J tiffs; gw;wpAk; njspthf $wg;gl;Ls;sJ.

nghJ FwpFzq;fs;

“ cz;lhFk; Ntisjd;dpy; NjfNeHik

cWjpaha;r; nrhy;YfpNwd; ed;wha;g; ghU

Fz;lhd Kfk;fz;fs; cjL ehf;F
Fwpg;ghd tha;NtWk; Njf Kw;Wk;
ntz;lhf NtAyHe;J ntz;ik ahfp
tpuy;efq;fs; KOtjpYk; uj;jk; tw;wp
fz;lhd fhy;fs;jhd; jzpe;J epw;Fk;
fUthd ehbaJ nkJtha;g; NghNk”
“NghNkjhd; jPgdq;fs; kl;Lg; gl;L
nghypthd fz;tpopfs; ngUj;Jj; Njhd;Wk;
MNkjhd; mrj;jpA khahrq; fz;L

5
 mtHeilAk; jsHe;J ngU%r;Rf; fz;L
%Nkjhd; %Hr;irAld; khh; Jbj;J
Kbthd fZf;fhypy; tPf;f Kz;lha;
J}Nkjh dpujaj;jpd; tjde; jd;dpw;
JUj;jpepfh; rj;jkJ Nfl;Fk; ghNu”
mfj;jpah; Fzthflk;

cjL Xuq;fspy; ntbj;jy;,

tha;g;Gz; : Stomatitis

fz; ntSj;jy; : Pallor of the eyes

cjL ntSj;jy; : Pallor of the lips

Kfk; ntSj;jy; : Pallor of the face

ehf;F ntSj;jy; : Pallor of the tongue

Njhy; tul;rp kw;Wk; ntSj;jy; : Pallor and dryness of the skin

grpapd;ik : Annorexia

glglg;G : Palpitation

Nrhk;gy; : Lassitute

NrhHT> kaf;fk; : Tiredness

,ja ehb Fiwjy; : Bradycardia

Ntiyapd; NghJ %r;Rj;jpzwy; : Dypnoea on exertion

tpop gpJf;fk; : Protrusion of eye balls

fZf;fhy; tPf;fk; : Ankle oedema

JUj;jp epfH xyp : Added heart sound in pericardium

6
 REVIEW OF LITERATURE

SIDDHA ASPECT

1. SIDDHA PHYSIOLOGY

rpj;jkUj;Jt mbg;gilapy; clypay; jj;Jtf; fzpg;gPlb

; idf; fzpg;gpl
gpd;tUk; fhuzpfs; Kf;fpa gq;fhw;Wfpd;wd.

 96 jj;Jtq;fs;
 07 clw;jhJf;fs;
 14 Ntfq;fs;
 04 cly; jP
1.1 . njhz;Z}w;whW jj;Jtq;fs;

“ cWjpahk; G+jhjp Nahiue; jhFk;

caHfpd;w nghwpiae;J Gyide; jhFk;
fWjpaha; fd;ktpe; jpupa ike;Jk;
fbjhd Qhdtpe; jpupa ike;Jk;
jpWjpahe; jPjha fuzk; ehd;Fk;
jpwkhd twpnthd;Wk; ehb gj;Jk;
kWjpahk; thAtJ gj;J khFk;
kfj;jhd tp\akQ;R Nfhr kQ;Nr”

“ mQ;rNt ahjhu khW khFk;

mwpa kz;ly%d;W ky%d; whFk;
njhQ;rNt Njhl%d;wpwP lizjhd; %d;W
Njhjkhq; Fz%d;W tpidap uz;lhk;
jQ;rNt uhfnkl;L ttj;ij iae;J
jaq;fpaNjhH fUtpflhk; njhz;Z}w; whW
xQ;rNt naht;nthd;wha; tpupj;Jr; nrhy;Ntd;
cWjpahk; G+jhjp Aiuf;ff; NfNs” ( A+fprpe;jhkzp )
A+fprpe;jhkzpapy; $wpagb

Kjy; jj;Jtk; 30
,uz;lhk; jj;Jtk; 30
%d;whk; jj;Jtk; 36
vd;wthwhf 96 jj;Jtq;fSk; tifg;gLj;jg;gl;Ls;sd.
7
1.2 cly; jhJf;fs; 07
ekJ cly; VO cly; jhJf;fshy; cUthdJ. rhuk;> nre;ePH> Cz;>
nfhOg;G> vd;G> %is > Rf;fpyk;, RNuhzpjk;. ,e;j VO jhJf;fSk;
clypid ed;dpiyapy; itf;f cjTfpd;wJ.

“ ,urk; cjpuk; ,iwr;rp Njhy; Nkij

kUtpa tj;jp thOk; nghL kr;ir

gutpa Rf;fpyk; ghohk; cghjp
cUgk yhYly; xd;nwdyhNk ” - jpUke;jpuk; 2086

clw;fl;Lf;fspy; nre;ePH cUthf;fk;

nre;ePh; gpj;jj;jpd; gz;Gfisf; nfhz;lJ. clk;gpy; Vw;gLk; tsHr;rpapy;
khw;wj;jpw;F mbg;gilf; fhuzkhf ,Ug;gJ FUjpjhd;.

,iug;igapy; nrupkhdk; eilngWk; NghJ rhuk; Kjy; ehspy;

cUthFk;. gpd; ,uz;lhk; ehspy; rhuk; nre;ePuhf cUkhWk;. %d;whk; ehspy;
Cdhf khWk;. ehd;fhk; ehs; nfhOg;ghf khWk;. gpd; Ie;jhk; ehs;
vYk;ghfTk; Mwhk; ehs; %isahfTk; Vohk; ehs; Rf;fpyk; my;yJ
RNuhzpjkhfTk; khWk;.

Kjypy; cUthFk; rhuk;> nre;ePH Mfpait clk;gpy; Cd;> euk;G

cz;lhfTk; vYk;Gfs; td;ikailaTk; fhuzkhfTk; ,Uf;Fk;. mit
khw;;wkilAk;NghJ cly; jhJf;fs; khw;wkilfpd;wJ. ghz;L Nehapy; rhuk;>
nre;ePH ghjpg;gilfpd;wJ. rhuk; ghjpg;G mile;J clw;NrhHT> %r;Rj;jpzwy;
cz;lhFk;. nre;ePH ghjpj;J cly,; fz; ntSf;Fk;.

1.3 Ntfk; 14
“ gjpdhd;F Ntfg; ngaHfs;
gfHe;jplNt mtw;iwf; Nfsha;
tpjpj;jpLk; thjk; Jk;ky;
NkTePH kyk; nfhl; lhtp
fjpj;jpL grpePH Ntl;if
fhrNkh bisg;G epj;jpiu
kjpj;jpL the;jp fz;zPH
tsHRf;fpyQ; RthrkhNk”

8
 1.4 cly; jP ehd;F
 rkdhf;fpdp
 ke;jhf;fpdp
 jPf;rhf;fpdp
 tp\khf;fpdp

ghz;L Neha;
NtW ngaHfs;
ntSg;G Neha;> ntz;ik Neha;> ntz; ghz;lk;

,ay;

 ,aw;if epwk; khwp cly; ntSj;J fz;izAk; eff; fz;izAk; ePf;fpg;

ghh;f;fpd; FUjpapd;wp ntSj;jpUf;Fk;.

Neha; ehly; Neha; Kjy; ehly; gFjp-2

 Njfj;jpd; ,uj;jj;jpy; cs;s rpte;j mZf;fs; Fiwe;J Njfk; ntSj;J

tpLtjw;F ghz;L Neha; vd;W ngah;. ghz;L Neha; ,uj;jk; nfl;L gythwhd
Neha; NrHtjhy; cz;lhfpd;wJ.

Mj;kul;rhkpHjk; gf;fk; 522

 moy; Fw;wk; kpFe;J gpj;jj;jpd; tiffshd mdw;gpj;jk; kw;Wk; ,uQ;rf

gpj;jk; ,tw;iwf; Nflilar; nra;J FUjpapd; epwj;ijAk;> viliaAk;
nfLj;J clYf;F Ntz;ba Cl;lj;ijAk; nfhlhky; cliy ntSf;fr;
nra;Ak; Neha;.

“ thnkd;w Nkdpnay;yh kQ;rspj;J kfh ntSg;G

cz;lhfp ke;jf; fz;zha;”

gjhHj;j rpe;jhkzp

 ghz;L NuhfkhdJ khHG mjpuy;> ruPuk; mNuhrpfk;> kQ;rs; epwkhd rpWePH>

tpaHit> ke;jhf;fpdp> Njfk; ,isj;jy;> ntSj;jy;> Mahrk;
vd;Dk; ,f;Fzq;fisj; jdf;F ,ay;ghfg; ngw;wpUf;fpd;wd.

rpfpr;rh uj;d jPgk;

9
 ghz;L Nehapd; tiffs;
rpj;jkUj;Jt E}y;fspd; mbg;gilapy; ghz;L Nehapd; tiffs;
gythwhf tifg;gLj;jg;gLfpd;wd. mit tUkhW>

1. mfj;jpaH Fzthflk ; 05
 thjg; ghz;L
 gpj;jg; ghz;L
 fgg; ghz;L
 kpUj;jpf ghz;L
 tp\g;ghz;L

2. A+fp rpe;jhkzp 800 06

 thjg; ghz;L
 gpj;jg; ghz;L
 fgg; ghz;L
 Kf;Fw;wg; ghz;L
 tp\g; ghz;L
 kz;Zz; ghz;L

3. jd;te;jpup itj;jpak; 07
 thjg; ghz;L
 gpj;jg; ghz;L
 fgg; ghz;L
 Kf;Fw;wg;ghz;L
 gpj;jthjg; ghz;L
 rd;dpthjg; ghz;L
 igj;jpag; ghz;L

4. T.V rhk;grptk;gps;is 06
 thjg; ghz;L
 gpj;jg; ghz;L
 fgg; ghz;L
 Kf;Fw;wg; ghz;L
 CJ ghz;L
 ePHg; ghz;L

10
5. itj;jpa rhu rq;fpufk; 05
 thjg; ghz;L
 gpj;jg; ghz;L
 %yg; ghz;L
 %ygpj;jg; ghz;L
 tplg; ghz;L

6. guuhrNrfuk; 05
 thjg; ghz;L
 gpj;jg; ghz;L
 fgg; ghz;L
 rd;dpg; ghz;L
 kpUjpfhg; ghz;L

7. kjiy Neha; kUj;Jtk; 05

 thjg; ghz;L
 gpj;jg; ghz;L
 rpNyw;gdg; ghz;L
 ,uj;jg; ghz;L
 mrhj;jpag; ghz;L

8. Nuhf epHza rhuk; 05

 thjg; ghz;L
 gpj;jg; ghz;L
 fgg; ghz;L
 Kf;Fw;wg; ghz;L
 tplg; ghz;L

9. mDNghf itj;jpa Njt ufrpak; 06

 thjg; ghz;L
 gpj;jg; ghz;L
 fgg; ghz;L
 Kf;Fw;wg; ghz;L
 tplg; ghz;L
 kpUj;jpfhg; ghz;L

11
10. [Pt uf;rhkpHjk; 05
 thjg; ghz;L
 gpj;jg; ghz;L
 fgg; ghz;L
 jpupNjhrg; ghz;L
 kpUjpfhg; ghz;L

11. ruNge;jpu itj;jpaKiwfs; ghz;L fhkhiyr; rpfpr;ir 05

 thjg; ghz;L
 gpj;jg; ghz;L
 fgg; ghz;L
 rd;dpghjg; ghz;L
 kz; jpd;wjhy; Vw;gl;l ghz;L

12. rpfpr;rhuj;d jPgk; 05

 thjg; ghz;L
 gpj;jg; ghz;L
 rpNyj;Jkg; ghz;L
 jpupNjhrg; ghz;L
 tp\g; ghz;L

2. SIDDHA PATHOLOGY
Neha;ehly;
rpj;j kUj;Jt Kiwapy; Nehapid Kf;Fw;w mbg;gilapy;> thj>
gpj;j> fgkhfg; gpupj;Js;sdH. ekJ kUj;Jt Kiw #f;Fk clYf;Fk; J}y
clYf;Fk; kUj;Jt topKiw te;Js;sJ.

2.1 ghz;L Neha;j; Njhw;wj;jpd; Kjw; fhuzk; - gpj;jk;

ghz;LNeha; tu Kjy; fhuzkhf ,Uf;Fk; Fw;wk; gpj;jkhFk;. vdNt
gpj;jj;ijg; gw;wp tpupthf ,q;F tpsf;fg;gLfpd;wJ.

gQ;r G+j mbg;gilapy; ,J jPapd; $W. eykhd clypy; ehb thjk;:

gpj;jk;: fgk; 1: 1/2: ¼ vd;wthW ,Uf;Fk;. cztpy; Vw;gLk; khw;wk;>
Rw;Wg;Gw #o;epiy khw;wk; vd;gdtw;wpdhy; gpj;jk; khw;wkile;J> eykhd
gpj;jj;jpd; tpfpjj;jpy; khw;wk; Vw;gLk; NghJ> gpj;j Nehahfpa ghz;L Neha;
cz;lhFk;.
12
 gpj;jk; clypy; ,Uf;Fk; ,lk;
gpq;fiy. ePh;g;ig> Koq;if. ,Ujak;> jiy> ce;jp> nfhg;G+s;>
gpuhzthA> ,iug;ig> tpaHit> ehtpy; CWk; ePh;> fz;> Njhy;. rhuk;> nre;ePh;.

nghJf; FwpFzk;

 ntg;gk;
 $Hik
 nea;g;G
 nefpo;rr; p
gpj;jk; ve;jg; nghUSld; NrUfpwNjh mJ mjd; Fzj;ij milAk;.

,aw;iff; Fzq;fs;

 nrupj;jy;
 td;ik
 ntk;ik
 nkd;ik
 ghHit
 ePHNtl;if
 grp
 xsp
 Rit
 epidg;G
 mwpT

gpj;jk; td;ikailAk; NghJ Vw;gLk; Fzq;fs; > vjpHf;Fzq;fs;

Fzq;fs; vjpHf;Fzq;fs;

 mf;fpdp FspHr;rp
 Gspg;G ,dpg;G
 CWk; jd;ik epiyj;jpUj;jy;
 fhuk; ifg;G
 F&uk; rhe;jk;
 ry&gk; nfl;b

13
 gpj;jj;jpd; njhopy;fs;
1. clypw;F kQ;rs;> nre;epwk; nfhLj;jy;
2. cly; ntg;gj;ij mjpfupf;Fk;
3. nrupkhdj;jpy; cly; ntg;gj;ij mjpfupj;jy;
4. tpaHit cz;lhf;fy;
5. ,uj;jj;ij mjpfupj;jy; kw;Wk; ntspj;js;sy;
6. Gspg;Gr;Rit jUjy;
7. Nfhgk;> epiyapy;yhJ ,Uj;jy;
8. fz;> kyk;> rpWePUf;F kQ;rs; epwk; jUjy;

Ritabg;gilapy; – gpj;jk;

cg;G jP ePH

Gspg;G kz; jP

fhHg;G fhw;W jP

cg;G> Gspg;G> fhHg;G jPapd; $W ,Ug;gjhy; gpj;jj;ij mjpfupf;Fk;.

vdNt ,jw;F ntg;g tPupak; ,Uf;Fk;.

“ GspJtH tpQ;Rq;fwp ahw;G+upf;Fk; thjk;

xspAtH ifg;Ngwpy; gpj;jQ;rW

P k; - fpspnkhopNa

fhHg;gpzpg;G tpQ;rpw; fgk; tpQ;RQ;rl;b ujQ;

Nrug; GzH NehaZfhNj” - fz;Zrhkpak;

JtHg;G> ,dpg;G> ifg;G> gpj;jj;ij rkd;gLj;Jk; Ritfs;> ,jw;F rPj

tPupak; ,Uf;Fk;.

“gpj;jkjp fupg;gpd; NgRk; gupfhuk;

Rj;jj; JtNuhL nrhy;ypdpg;Gr; rj;jhFk;

ifg;Gr; RitNa fUJtjd; tPW

va;GilA nkd;Wiuj;jhupq;F” - fz;Zrhkpak;

gpj;jk; NflilAk; NghJ JtHg;G> ,dpg;G> ifg;G RitAila

kUe;JfisNa nfhLj;jy; Ntz;Lk;.

14
 2.2 Kf;Fw;w NtWghL
cly; td;ik Fiwe;J grpj;jP (mdw; gpj;jk;) Nflile;J cz;l czT
rupahf nrupahky; NghFk;.

cztpd; Nfl;lhy; ,ur FUjpfSf;F Cl;lk; ngwhJ .( ,uQ;rf gpj;jk;)

NjhYf;F epwj;ijf; nfhLf;Fk; moy; nkype;J epwj;jpYk; vilapYk;

Fiwe;J jPf;Fw;wj;ijg; ngUf;Fk;. (gpuhrf gpj;jk;)

mjdsthf kw;iwa Fw;wq;fSk; jd;dpiyapy; jpupe;J guTfhypd;

td;ikiaf; nfLj;J Nehia cz;lhf;Fk; (tpahdd; ghjpg;gilfpd;wJ)

Nehapd; td;ik ngUfg;ngUf IaKk; ngUfp tPf;fk; KjypaitfisAk;

Jiznfhs;sr; nra;Ak;.

 thjk;
thjk; thOkplk;
mghdd;> kyk;> ce;jpapd; fPo; %yk;> euk;Gf; $l;lk;> Cd;> gf;Fthrak;>
fhJ

,aw;ifg; gz;G

 Cf;fKz;lhf;fy;
 %r;Rtply; thq;fy;
 kdnkhop nra;fSf;Fr; nraiyj;juy;
 kyk; Kjypa gjpdhd;F tpiuTfis ntspg;gLj;jy;
 rhuk; Kjypa VO clw fl;Lfl;Fk; xj;j epfo;rr
; piaj;juy;
 Ik;nghwpfl;F td;ikiaf; nfhLf;Fk;.

tiffs; 10
1. gpuhzd;
ghz;L Nehapy; %r;Rtpl rpukk;> czT nrupahik Vw;gLk;
2. mghdd;
ghz;L Nehapy; cztpd; rhuk; NruNtz;ba ,lq;fspy; NrHg;gpf;fhJ.
fopr;ry; kyf;fl;L rpWePh;f; FiwT Vw;gLk;.
15
 3. tpahdd;
ghz;L Nehapy; cly; tPf;fk;> fz; cjL ntSj;jy; cz;lhFk;.
4. cjhdd;
ghz;L Nehapy; mjpf ePH Ntl;if cz;lhFk;.
5. rkhdd;
ghz;L Nehapy; grpapd;ik Vw;gLk;
6. ehfd;
,ay;G
7. $Hkd;
,ay;G
8. fpUfud;
grpapd;ik cz;lhFk;
9. Njtjj;jd;
ghz;L Nehapy; J}f;fkpd;ik cz;lhFk;
10. jdQ;nrad;
ghz;L Nehapy; ghjpg;gilahJ.

 gpj;jk;
gpj;jk; thOkplk;
gpq;fiy> ePHg;ig> Koq;if> ,Ujak;> jiy> nfhg;G+o;> ce;jp>
gpuhzthA> ,iug;ig> tpaHit> ehtpy; CWk; ePH> nre;ePH> ruk;> fz;>
Njhy;.

1. mdw;gpj;jk;
ghz;L Nehapy; grpapd;ikia cz;lhf;Fk;
2. gpuhrf gpj;jk;
ghz;L Nehapy; fz;> Njhy; ntSj;jy;
3. ,uQ;rf gpj;jk;
ghz;L Nehapy; fz;> Njhy; ntSj;jy;
4. MNyhrf gpj;jk;
,ay;G
5. rhjf gpj;jk;
ghz;L Nehapy; njhopy;ruptu nra;aKbahky; cly; NrhHT cz;lhjy;.

16
 fgk;
,Uf;Fkplk;
rkhdthA> tpe;J> jiy> ehf;F> nfhOg;G> vYk;G k[;i[> FUjp> khHG>
%f;F> euk;G> vYk;G>%is> fz; kw;Wk; %l;Lf;fs;.

1. mtyk;gfk;
ghz;L Nehapy; %r;Rj; jpzwy; cz;lhFk;.
2. fpNyjfk;
ghz;L Nehapy; grpapd;ik cz;lhFk;.
3. Nghjfk;
ghz;L Nehapy; grpapd;ik> Ritapd;ik cz;lhFk;
4. jw;gfk;
,ay;G
5. re;jpfk;
,ay;G

2.3 gUt fhyq;fs;

gpj;jk; jd;dpiy tsHr;rp kw;Wk; Ntw;Wepiy tsHr;rpailAk;

fhyq;fshf gUtfhyq;fspy;> fhh;fhyk; kw;Wk; $jpH fhyk;
fhzg;gLfpd;wd.

TABLE - 01

Fw;wq;fs; jd;dpiy Ntw;Wepiy jd;dpiyailjy;

tsh;r;rp tsHr;rp
tsp KJNtdpy; fhH fhyk; $jpH fhyk;
fhyk;
moy; fhH fhyk; $jpH fhyk; Kd;gdpf; fhyk;
Iak; Kd;gdp fhyk; ,sNtdpy; KJNtdpy; fhyk;
fhyk;

2.4 epyk;
FwpQ;rp> nea;jy; kw;Wk; ghiy epyq;fspy; thOk; kf;fSf;F ghz;L Neha;
tUtjw;fhd tha;g;Gf;fs; mjpfk;.

17
3. SIDDHA PATHOGENESIS

3.1 Neha;tUk; top (AETIOLOGY)

In this disease due to intrinsic and extrinsic cause. Uyirthathu (Vatham,

Piththam, Kapam) and Udal thathu (Saram, Senner, Ooon, Kozhuppu, Enpu,
Moolai and Sukkilam/Suronitham) get deranged.
Especially, in Uyir thathu, initially Kapham gets altered and then other two
thathus are changed.
In Udal thathu, the derangements occurs in order. Initially Saram, then Seneer
and so on.
 mfj;jpaH Fzthflk; vd;w E}ypy; Neha;tUk; top njhlh;ghf gpd;tUkhW
$wg;gLfpd;wJ>

“Njulh Njfj;jpy; ,uj;jk; tw;wpj;

jPq;fhd tpe;JNeha; fhZkg;gh
$wlh nrhy;YfpNwd; ed;wha; ghU
Fwpg;GlNd ePaijj;jhdwpe;J nfhs;Ns” (21)

nfhs;slh mgf;Ft Nghrdj; jpdhYk;

Fb nfLj;j ngUk;ghL fpuhzpahYk;
fs;nslh fUg;gj;jpd; fpue;jpahYk;
fdkhd uj;jj;jpd; Nghf;fpdhYk;
ms;slh mjpahk ftdj;jhYk;
mstw;wtp rhue;jhd ilAk; NghJk;
njs;sNt Njfj;jpy; ,uj;jk; nfl;L
njspthd ghz;lJT Kz;lhk; ghNu (22)
mfj;jpaH Fzthflk;

Un healthy cooking methods, Negligent treatment for menorrhagia, Diarrhoea,

Fibroid uterus, Profuse bleeding leads to Paandu noi.

 A+fpKdp vd;w E}ypy; Neha;tUk; top njhlh;ghf gpd;tUkhW $wg;gLfpd;wJ

“ mwpe;JNk cw;gj;jp nrhy;yf; Nfsha;

mjprhu kykpsfp nae;Ne ue;jhd;
gpwpe;JNk GspAg;G ngUj;jyhYk;
18
 ngj;jkh kf;fpdpap ypUj;jyhYk;
kpwpe;JNk jhk;G+y kpf mUe;jyhYk;
kPwpNa kJf;fisj; jhd; Grpj;jhYk;
gwpe;JNk gfy; epj;jpiuNa nra;jyhYk;
ghz;L te;J ghupYs;NshH gLk; ghlNk”

“ ghlhd gQ;R jidj; jpUb NdhHf;Fk;

ghq;fhd rptJapiyj; jpUb NdhHf;Fk;
khlhd gRtijg; gl;bdpahf
itf;fpd;NwhH kwtopapy; ele;jplhjhH
fhlhd thuzpae; jzpw;g wj;Jf;
fLtijfs; nrapfp;d; NwhHfz; fhzhjh
Nfhlhd gop nrhy;ypf; FbnfLf;Fk;
nfhLk;ghtp ghz;L tpdhw; Fwp nfhs;thNu”
- A+fp rpe;jhkzp

The above stanza explains frequent attack of diarrhea, excessive intake

of salt and sour food, living in hot surroundings, excessive chewing of betel leaves
and nuts, excessive alcohol intake, sleeping in the day time, stealing the temple
properties ect..

The above same causes are explained in “ Chinthamani ennum

vaiththiya nool” and “Roga nirnaya sarum ennum roga nithanam” by T.R .
Mahadeva pandithar and “ madhava nithanam” by Durai samy Iyangar and
“ Jeeva Raksamirtham”

 mfj;jpaH thflk; vd;w E}ypy; Neha;tUk; top njhlh;ghf gpd;tUkhW

$wg;gLfpd;wJ>

“ehnkd;w nrhy;YfpNwhk; ghz;L te;j

eykhd fUkkJ nrhy;yf; NfS
jhnkd;w jha;je;ij kdk; Nehfr; nra;jhy;
juzpjdp Ys;s thf;Fk; md;Ng nrhy;y
thnkd;w tpUg;gopj;jy; nrtp Rthr
kw;Wk; ngha; nrhy;yyhq; fhuQ; nra;jy;
Ntnkd;w fUkkJ gpj;jNkwp
ntWj;jjlh ntg;G kpQ;rpf; iffhNyha;Nt”
- mfj;jpaH thflk;
19
 Disobedience to the parents and other people, speaking lies, getting angry with
others will others will produce warmness of the body, fatigue which may leads to
Pandu noi.
 jd;te;jpup itj;jpak; vd;w E}ypy; Neha;tUk; top njhlh;ghf
gpd;tUkhW $wg;gLfpd;wJ

“jpUe;jpLk; ghz;L Nuhfq; NrHj;jpLq; Fzj;ijf; Nfsha;

,Uj;jpLk; thj gpj;jr; rpNyw;gd kpitjhd; khWk;
gupe;Jjh ndhd;Nwh nlhd;W nghUe;JtjhY kz;NzhL
mUe;JtjhYk; ghz;L mize;jpL nkd;dyhNk”

“Mfpa %ye;jd;dp yize;j Tl;lzj;jhYe;

NjhifaH Nkfj;jhUk; JaHkpF NrHjyhYk;
NjfNghrizAs;shHf;Fj; jupj;jpuQ; NrHjyhYk;
Ntf khe;jpupNjhUq;fs; kpQ;rpNa ghz;LthNk”

Imbalance between the three thathus Vatha. Pitha, Kapha perversion of

appetite in the form of geophagia, excessive heat accumulation due to altered
abana vayu, excessive sarrow, phycho social factors are some of the cause of
Pandu.

 FUehb vd;w E}ypy; Neha;tUk; top njhlh;ghf gpd;tUkhW

$wg;gLfpd;wJ

“taujdpw; G+ehf jd;idr; rhHe;J

tUj;jpaJ Gw;WNghw;g; gw;wpf;fhZk;

vOk;gpaJ fpUkpjh dpile;JGf;fpy;

,ay;ngUf;Fq; Fly; kltha; nrhy;yf;NfS”

Pathologically, blood loss may occur due to various causes. One among them
is worm infestation, which leads to chronic blood loss from the intestine – hence
causes Anaemia.

“ fpUkpahy; te;jNjhlk; ngUfTz;L

Nfl;fyjpd; gpuptjidf; fpufkhf

20
 nghUkptUk; thAnty;yhq; fpUkpahNy
GOf;fbNghy; fhZkJ fpUkpahNy

nrUkptUk; gTj;jpuq;fs; fpUkpahNy

Njfkjpy; Nrhiff; Fl;lk; fpUkpahNy

JUkptUQ; RNuhzpjq; fpUkpahNy

JUkptUQ; RNuhzpjq; fpukpahNy

Jl;rKld; fpupkpaijj; njhopy; nra;tPNu”

According to this Sobai will occur due to worm infestation which meant Pandu
noi.

 ghythflk; vd;w E}ypy; Neha;tUk; top njhlh;ghf gpd;tUkhW

$wg;gLfpd;wJ

“ gpwe;jehs; gps;isf;Fj; jhNd jd;wha;

gpjhthNy gpzpAlypd; NkNy Njhd;Wk;

fdyJ nkj;jf; fhZk; fz;zJ

ntSf;Fe; jhNd nrSj;jpL KjLjhDk;…”

“tpidaJ tUF NeHik tpgukh Aiuf;ff;Nfsha;

midaJ thfe;jhD kghddhk; thA$b

GidaJ fPo;Kyj;jpw; Gf;fpdhy; jbf;Fk; Njfk;

fdyJ nkj;jf;fhZk; fz;zJ ntSf;Fe;jhNd”

Congenital, neonatal diseases are due to parental factors. Pandu may also
occur as genetic disorders.

 T.V rhk;grptk;gps;is vd;w E}ypy; Neha;tUk; top njhlh;ghf

gpd;tUkhW $wg;gLfpd;wJ
rpy;nyd;W tPRk; FspH fhw;wpy; jpuptjhYk;> cl;fhHe;J my;yJ
gLj;Nj ,Uj;jyhYk;> Fz;bf;fha; Neha;> ,Ujak;> EiuaPuy;> kz;zPuy;>
Kjypa cWg;Gf;fisj; jhf;Fk; Neha; NfhshWfshYk;> kw;Wk;

21
 ngz;fSf;F khjtplha;f; NfhshwpdhYk; Vw;gLk;. ,e;Neha; gpwtp
NehahAk; ,Uf;fyhk;. Nkf rk;ge;jkhd fpue;jp Kjypa Neha;fs;> Nrhif
Neha; ,itfshYk; cz;lhfyhk;.
In his opinion, pandu means only venmai (pallor) refers merely to anaemia
where the patient turns pale or white.

 NjiuaHthflk; vd;w E}ypy; Neha;tUk; top njhlh;ghf

gpd;tUkhW $wg;gLfpd;wJ

“ fUjpa kPdpd; Ks;Sk; fye;Jkp nea;apy; thYk;

kUtpa vYk;Gq; fy;Yk; kq;ifaH kUe;jPLk;

gofpa goQ;Nrhw;whYk; goky epiwfshYk;

kUfpa kapHfshYk; te;jpLk; NehajhNk

Gwtiu Az;ifahYk; Nghf ePUz;ifahifahYk;

RusNt Klf;fpf; nfhz;L Kwf;fplf;ifahYk;

ngUf ntz;nlhopapdhYk; gpwf;fNehnad;Nw fhNz”

Therayar vaagadam says that thorns of fish , paady bran, bone, stones,old rice,
hair in food are the dietary factors causing Pandu. Then severe constipation,
drinking polluted water, sleeping in an abnormal posture are all the causes that
bring out Pandu noi.

 mfj;jpaH gupG+uzk;- 400 vd;w E}ypy; Neha;tUk; top njhlh;ghf

gpd;tUkhW $wg;gLfpd;wJ

“ ey;NyhHfs; ngupNahHfs; elj;JQ; nra;if

ehl;bYs;s JHFzq;fs; eifj;jhNy

nghy;yhj tp\ePH gw;wp te;J

Njfnky;yhk; F\;lk; NghyNt

nrhy;yhj fb tp\q;fs; Fd;kk; ghz;L”

Here it is explained that Pandu and other diseases occur due to the toxic
substance produced in the body by their unhealthy life style.

22
 gjpndz; rpj;jHfs; ehb E}y; vd;w E}ypy; Neha;tUk; top
njhlh;ghf gpd;tUkhW $wg;gLfpd;wJ

“mwpthd gpj;jj;jhnyLj;j NjfkJ nkypT

epwk; nts;is aupit NahL

gpupahj Rfypiy aw;gTz;L ngUk; Gspg;GzT

nfhs;s………”

The pitha Theghi may get emaciated and later the body becomes pale. More
over excess intake of sour food stuffs results in pandu noi.

 ruNge;jpu itj;jpa Kiwfs; (ghz;L Nuhf rpfpr;ir)

guje;jpu fhuzq;fspdhy; ghz;L cz;lhFk; tpjk;

 Mfhuj;jpy; g;uPjpapd;ikapdhy; Mfhuk; ruPuj;jpw;F NjitAs;sgb

rhg;gplKbtjpy;iy. MfNt u] jhJ FiwtJld; ,uj;jk;> khk;]k;> Kjy;
Rf;fpy jhJ tiu ruPu jhJf;fs; gytPdg;gl;L> ghz;L Nuhfj;ijAz;lhf;Fk;.
 [Puzf; NfhshW> ,yF Mfhuj;ij mjpfkhf rhg;gpl;lhNyh
my;yJ ];tghtkhd FU FzKs;s Mfhuj;ij (NfhJik> uit)
rhg;gpl;lhNyh mit rupahdgb rPuzpf;fg;glhky; “Mku]k;” cz;lhfp
uj;jk; Kjyhd jhJf;fspd; tsHr;rp jilg;gl;L ghz;L Nuhfj;jpw;F
fhuzkhfpd;wJ.
 fLikahd tpahjpapypUe;J tpLgl;l Nuhfp> jd; mf;dp gyj;ij mwpahky;
Mfhuj;ij cl;nfhz;lhNyh Mfhuk; rPuzkhfhky; uj;jk; rupahf tpUj;jp
Mtjpy;iy.
 uj;jk; FiwTgLjy;> r];jpu g;uNahfj;jpd; NghJ ,uj;jk; mjpfkhf tbjy;>
mbgl;L mjd; %yk; ,uj;jk; ntspahjy;> ,uj;j gpj;jk;> uj;j mjprhuk;>
uj;j Fd;kk;> uj;j gpujuk; Nghd;w Nuhfq;fshy; ,uj;jk; mjpfkhf ntspahfp
e\;lkiljy; Kjyhd fhuzq;fSk; ghz;L Nuhfj;ij cz;Lgz;Zk;.
ngz;fSf;F fHg;g];uhtk;> fh;gghjk; KjypaitfSld; gpurtfhyq;fspy;
Vw;gLk; mkpjuf;j];uhtKk; ghz;LTf;F fhuzq;fshFk;.
 uj;jk; J}\pj;JtpLjy;> <ak;> urk;> jhk;gpuk; Kjyhd cNyhfq;fis Rj;jp
nra;ahky; nre;J}uk;> gw;gk; Kjypaditfisr; nra;J cgNahfpj;jhy;
mit ,uj;jj;ij Kwpj;J ghz;L Nehia cz;lhfpd;wJ. tpfh]p
FzKs;s ghf;F Kjyhd jputpaq;fis mjpfkhf cgNahfpj;jhy; ,uj;jk;

23
 khWgl;L ghz;LNuhfj;ij cz;lhf;Ffpd;wJ. ,jid tp\g;ghz;L vd;Wk;
$Wth;.
 gjhHj;j Fzk; vd;w E}ypy; Neha;tUk; top njhlh;ghf
gpd;tUkhW $wg;gLfpd;wJ.

“ FwpQ;rp tUepyj;jpw; nfhw;w Kz;b uj;jk;

cwpQ;r tU RuKz;lhk; mwpQiuf;
ifaNk jq;F juj; jhikty;iy A+q;fjpHf;Fk;
IaNk jq;Fk; mwp”

There is an evidence that the Kurunchi nilam, the hills and its surrounding
areas are endemic for Pandu noi

 gjhHj;j Fz rpe;jhkzp vd;w E}ypy; Neha;tUk; top njhlh;ghf

gpd;tUkhW $wg;gLfpd;wJ

“ FwpQ;rptU epyj;jpw; nfhw;w Kz;b uj;jk;

cwpQ;rptU RuKz;lhk; mwpQUiuf;

ifaNk jq;Fjuj; jhik ty;yiyAq; fjpf;Fk;

IaNk jq;Fk; mwp”

 Neha; ehb Neha; Kjy; ehly; gFjp- 2 vd;w E}ypy; Neha;tUk;

top njhlh;ghf gpd;tUkhW $wg;gLfpd;wJ
nghJthf tsH ,sk; Foe;ijfs; FUjpapd; td;ikiaf;
Fiwf;ff; $ba cg;G Gspg;Gs;s nghUl;fis kpFjpahff; nfhs;tjhYk;>
Ruk;> Ngjp > the;jp> fPy;thA Kjypa Neha;fSf;Fl;gLtjhYk;> FUjpia
msT fle;J ntspahf;Fk; FUjpaoy; Neha;> FUjp fopr;ry;> Kis Neha;>
FUjp the;jp Kjypait Vw;gLtjhYk; ntl;Lg;gl;L kpFjpahff; FUjp
ntspg;gLtjhYk; ,e; Neha; cz;lhk;. md;wpAk; er;Rj;jd;ikAila
kUe;Jfis ehssTf;F kpQ;rp cz;gjhYk;> cliy ,isf;fr; nra;Ak;
tapw;Wg;GO Neha;> ,isg;G Neha;> epzf;fopr;ry; KjypaitfshYk;
FUjpngUf;iff; nfLf;ff;$ba <uy; Neha;fshYk;> Gifapiy> ntw;wpiy>
ghf;F> kz;> rhk;gy;> jpUePW> fw;G+uk;> Kjypaitfis mbf;fb
nfhs;tjhYk; ghz;L Neha; Vw;gLk;.

24
 3.2 ghz;L Neha; FwpFzq;fs;

3.2.1 Kw;FwpFzq;fs;

 mjpfkhd cly;NrhHT
 %r;Rtpl rpukk;
 fz;ghHit
 xspFd;wy;
 kaf;fk;
 khHG glglg;G
 cly; ntSj;jy;

vd;gd cz;lhf;Fk;.

3.2.2 nghJ FwpFzq;fs;

“ cz;lhFk; Ntisjd;dpy; NjfNeHik

cWjpaha;r; nrhy;YfpNwd; ed;wha;g; ghU

Fz;lhd Kfk;fz;fs; cjL ehf;F
Fwpg;ghd tha;NtWk; Njf Kw;Wk;
ntz;lhf NtAyHe;J ntz;ik ahfp
tpuy;efq;fs; KOtjpYk; uj;jk; tw;wp
fz;lhd fhy;fs;jhd; jzpe;J epw;Fk;
fUthd ehbaJ nkJtha;g; NghNk”

“NghNkjhd; jPgdq;fs; kl;Lg; gl;L

nghypthd fz;tpopfs; ngUj;Jj; Njhd;Wk;
MNkjhd; mrj;jpA khahrq; fz;L
mtHeilAk; jsHe;J ngU%r;Rf; fz;L
%Nkjhd; %Hr;irAld; khh; Jbj;J
Kbthd fZf;fhypy; tPf;f Kz;lha;
J}Nkjh dpujaj;jpd; tjde; jd;dpw;
JUj;jpepfh; rj;jkJ Nfl;Fk; ghNu”
- mfj;jpah; Fzthflk;

mfj;jpaH Fzthflj;jpd; gb cjL Xuq;fspy; ntbj;jy;> tha;g;Gz;>

fz; ntSj;jy;> cjL ntSj;jy;> Kfk; ntSj;jy;> ehf;F ntSj;jy;>
Njhy; tul;rp kw;Wk; ntSj;jy;> grpapd;ik> glglg;G> Nrhk;gy;> NrhHT>

25
 kaf;fk;> ,ja ehb Fiwjy;> Ntiyapd; NghJ %r;Rj;jpzwy;> tpop
gpJf;fk;> fZf;fhy; tPf;fk;> JUj;jp epfH xsp vd;gd cz;lhFk;.
 ,e;Nehapy; cly; td;ik ehSf;F ehs; Fiwe;J elf;f ,ayhik> jiy
Nehjy;> kaf;fKz;lhjy;> %r;Rj;jLkhwy;> grpj;jP nfly;> czT
Ntz;lhik> cz;l rpW czTk; the;jpahjy; Mfpa Fwpfs;
Njhd;Wk;. ,d;Dk; kpfTk; ntSj;Jj; Njhy; RUf;fy;> cly; nkype;J
gsgsj;J ntSg;ghjy;> eff; fZf;fs; jbj;J ntSj;jy;> eh ntbj;Jg;
Gz;zhjy; my;yJ ehtpd; Nkw; Njhiyr; rPtpnaLj;jJ Nghd;W
rPtpnaLj;jJ Nghd;W rpte;J fhZjy;> njhz;il fl;Ljy; vd;Dk;
FwpfSk; fhZk;.

- A+fpKdp itj;jpa rpe;jhkzp

 rUk ntbg;G> mbf;fb fhwp ckpo;jy;> Njfk; nkypjy;> kz; rhg;gpLtjpy;
tpUg;gk;> fz;fisr;Rw;wpYk; tPf;fk;> kyk; %j;jpuk; Kjypaitfs; kQ;rs;
epwkiljy;. rhg;ghL ed;whfr; nrupahik Kjyhd Fwpfs; Vw;gLk;.

- ruNge;jpuH itj;jpa Kiwfs;

 “ cw;wNjhH md;dNgjk; mNuhrfk; Kjuke;jk;
Kw;wpkhHG Neha; %j;jpuk; nghd;dpd; td;ik
nts;spNrH Gwq;fhy; iftPf;fKly; ntSj;jy;
NtHj;jy;gw;wp njhf;fpw;fha; gzpj;jpa ghz;LthNk”

-mfj;jpaH itj;jpa uj;jpdr; RUf;;fk;

mfj;jpaH itj;jpa uj;jpd RUf;ff; $w;Wg;gb grpapd;ik> khHG typ> rpWePH

epwk; khw;wk;> fZf;fhy; tPf;fk;> fz;,iug;ig tPq;fy;> cly; ntSj;jy;
cz;lhFk;.

 “ nrlkJ gpj;j ePuhy; njspj;jjhy; Njf nkq;Fk;

flkJ fdf;f T+jpf; fz;ZNk ntSf;Fe; jhNd
ntSj;jpL kpuz;lhd; lhdhy; tpidao #of; Nfsha;
fisj;jpL rlye; jd;dpy; fdyjha; twl;rp fhZk;
gOj;jPLe; Njf %jpg; ghz;L Nghyhk”

-ghythflk;

ghythflj;jpd; $w;Wg;gb> fz;nts; tpop ntSj;jy;> cly;twl;rp> cly;

NrhHT> tPf;fk; cz;lhFk;.

26
 3.3; rpj;j kUj;Jt E}y;fspd; mbg;gilapy; Neha;
FwpFzq;fs;

3.3.1 mf];jpaH Fzthflk;

 thjg; ghz;L
“ ifAq; fhYq; fUj;JisAq; fz;Zq;ifAk; KfKk; tauijf;Fk;
nka;Ae; jsHe;J ntSj;jpUf;Fk; ntz;zpDiuaha; thdpA
ka;Aq; Nfhgpj;jpisg; Gz;lhad;dQ; NrHe;J the;jpf;Fk;
ca;a thjghz;Lntd ciuj;jhH ngupNahUiuj;jhNu”

“ke;jk; gj;J KjH Kstha;ePH ngUj;J the;jpf;FQ;

re;JjhS nkhop nghWj;J jhe;J Ke;jpf; fUj;JisA
Ke;JkfOkijg; Gz;lh%r; Nrhbisg;G tpf;fYkhk;
,e;jf; FzNkapUe;J njd;wy; thjghz;Lnad tpok;Ngd;”
 Pain in the extremities and abdomen
 Oedema of eyes, face and arm
 Pallor of the body
 Lassitude
 Dyspnoea
 Vomiting
 Hic cough
 Excessive salivation
 gpj;jg; ghz;L

“ fz;Lnfhs; ePNajpNufk; efk; %j;jpuk;

fUj;Jld; kQ;rsha;f; fhl;L ka;ah

Jz;bdpy; gl;l %j;jpuf; fiwAe;jhd;

gRik epwq; fz;L fhl;Lq; fhNz.” 230

“fhzlh kyk; ntSj;Jf; fspkz; Nghyf;

fdj;j jpNufj;jpy; eikr;ry; fhZk;

Ntz;bakl;Lk; Mahrk; J}f;f kaf;fkld;

Nfhgk; te;J Njhd;Wk;” 231

27
 “ Njhd;Wk; tha;f;frg;G NkjpAw;w ehbAk;

Njhd;wpLk; fz;fSk; kQ;rshFk;

aPd;wNjhH %isAk; nfl;Lg; Gj;jpkhwp

,isf;FNk jpNufe;jhd; f\zj;Jf;Fs;Ns 232

“f\zj;Jf;Fs;Ns jPHj;jpl kUe;J Nfsha;

nrhy;Ntd; nrayhd Ngjp fPa;e;jhahdhy;

gzg;ig Nghnyhj;j gpj;jg; igf;Fs;jhd;

gspr;nrd;W fPo;Nehf;fp tpOFk; ghNu” 233

 Yellowish colouration of the body, eyes,nail and urine

 Mood swing loss of intelligence
 Pallor of the stool
 Body itching
 Tiredness
 Memory loss
 Dyspnoea
 Giddiness
 Lassitude
 Bitter in taste
 Emaciation

 fgg; ghz;L

“nka;aNt tOf;Fk;tauijf;Fk; tPq;Fk; gpwq;fhy; gpwq;iffs;

iffhNyhAq; fpUfpapUf;Fk; fz;Zk;KfKk; gQ;rhFe;

Ja;ajha ky ePuhae;J tpOe; njhz;il rpjWe; Jg;GkpspH

ka;akpf;F kpf; Fzq;fs; NrHg;gd ghz;L khFkpNj”

28
 “ Nth;j;J ntJk;Gq; fz;FspUk;Ntr; nrd;wpUf;Fk; tpyhTk; neQ;Rkhj;

Jkplh Nghybf;Fk; mJ ma;ak; gpj;jq; fye;J tUk;

jpHf;fkd;wp kbAz;lhjpj;jpdhTk; tOtOf;Fk; ghH

jhSlk;G tPf;fKk; NrHg;gd ghz;L ntdg; gfNu”

 Shining of the skin

 Abdominal flatulence
 Oedema of feet
 Odema of the dorsum of the hand
 Abdominal swelling
 Swelling of tongue
 Lassitude
 Giddiness
 Husky voice
 Pallor of the eye, face, urine and faeces
 Excessive sweating
 Chillness of eyes
 Thoracic Pain
 Anasarca
 Chest pain
 kpUj;jpf ghz;L

“ghNueP ky%j;jpuk; ahT ka;ah

gz;ghf kQ;repwj; jpwq;F kg;gh

$NweP kpUj;jpfh ghz;bd; NeHik

FzKlNd nrhy;YfpNwd; Fwpg;gha;f; NfS

NjNueP jpj;jpg;G kz;Zq; $l

jpukhd JtHkz;ZQ; rTl;L kz;Zk;

jPuhffj; jpde;jpdKe; jpd;W te;jhy;

jPukhd kpUj;jpfh ghz;Lz;lhNk.” 25

29
 “ cz;lhFk; NghjpdpNy Njf NeHik

cWjpaha; Kd;nrhd;d Fzj;ijf; fhl;Lk;

gz;lhf ,JjPu kUe;J nrhy;Ntd;

gFj;jnjhU ghtdey; NyhfKe; jhd;

ez;lhd yFtpNuh rdK khFk;

eykhd Njfj;jp nyy;yhk; tPq;Fk;

Jz;lhd fpUkpkyk; uj;jq; Nfhio

Jyq;Fklh ,e;Neha;f;F Fze;jhd; ghNu.” 26

 Yellow colouration of urine, stool

 Indigestion
 Flatulence
 Vomiting
 General oedema
 Bacillary dysentery

 tpr ghz;L

“ tpjp jPHe;j Nuhfklh tplg;ghz; la;ah

tpgukha;r; nrhy;YfpNwd; tprpjq; Nfsha;

kjpNghd;w NjfkJ ntSj;Jf; fhl;Lk;

kjpnfl;L kpFRuKe NjhlKz;lha;r;

rjpnra;A
; k; the;jptpf;fy; ,Uky; fz;L

rjpuhf tpNuhrpfj;ij Az;L nra;J

mjpfkha;j; Njfj;jpy; tPf;fKz;lha;

md;dj;ijj; js;sptpL ktdp NahHf;Nf.” 28

 Pallor of the body

 High fever
 Vomiting

30
 Hic cough
 Cough
 Hallucination
 General oedema
 Anorexia

3.3.2 A+fpitj;jparpe;jhkzp
 thj ghz;L

“nfhs;sNt thjg; ghz;L Nuhfk; Nfsha;

Fly;Gul;b mbtapWjhd; typf;Fk;

js;sNt jhfnkhL grpAkpy;iy

joyhd rurug;ghfj; jhDk;

ey;yNt euk;ngy;yhk; fWg;GkhFk;

eLf;fnyhL fz; rptg;G kyge;je;jhd;

tps;sNt jiytypf;Fk; Nkdp tPq;Fk;

ntSg;ghFk; thjj;jpd; ghz;LjhNd.”

 Pain in the lower abdomen

 Thirst
 Loss of appetite
 Dryness of the skin
 Vein become more visible due to pallor of the skin
 Rigor
 Redness of the eye
 Constipation
 Headache
 Pallor of the skin and anasarca.

 gpj;jg; ghz;L

“thnkd;w Nkdpnay;yhk; kQ;rspj;J

kfhntSg;G cz;lhfp ke;jf; fz;zhw;

31
 jhnkd;w jhfnkhL %Hr;irahFe;

jdpthapy; kpsF Nghw; whDiuf;Fk;

Nenkd;w neQ;rKb jhDKz;lha;

neUf;fpNa %r;R Kl;lJNt ahFq;

Nfhnkd;w fpWfpWj;J tha; ifg;ghFk;

fpsH gpj;jg; ghz;L ntdf; $wyhNk.”

 Yellowishness and pallor of the skin

 Diminished vision
 Severe thirst
 Fainting
 Pungent taste like pepper
 Chest pain
 Dyspnoea and giddiness
 Bitter taste

 fgg; ghz;L
fPwpaNjhH euk;GNjhy; kpf ntSg;G

fpsh;ehT cg;Giwf;F kapH $r;rhFk;

thwpaNjhH the;jpahq; FuYq; fk;Kk;

kfj;jhd Jk;kYld; NfhioahFk;

<wpaNjh upUknyhL kaf;f Kz;lh

kpLg;grjp ape;jpupa el;lkhFQ;

rPwpaNjhH NrhgnkhL jhf khFQ;

rpNyl;Lkj;jpd; ghz;nld;dr; nrg;gyhNk.”

 Pallor of the skin

 Salty taste
 Horripillation
 Vomiting
 Husky voice

32
 Sneezing
 Cough with expectoration
 Fainting
 Lassitude
 Emission of semen

 Kf;Fw;wg; ghz;L

“ nrg;gNt mUrpnahL Nrhgjhfk;

nrayhd RthrnkhL ,isg;GkhFk;

ntg;gNt NkeprpWePH jhd; tpOk;

kpLf;fhd gy<dkhdhH gpbj;jy;

Ja;aNt #l;NlhL jpaf;fkhFe;

Jk;k yhAlk; ngq;F %jPf; fhZ

jpg;gNt Njfnkq;FkrjpahF

jpupNjhrg; ghz;nld;dr; nrg;G E}Ny

 Anorexia
 Anasarca
 Dyspnoea
 Emaciation
 Hot urine
 Lassitude
 Chest pain
 Warmness of the skin
 Sneezing
 Weakness

 tprg;ghz;L

“ E}yhf efj;NjhNl Aly; ntSf;Fk;

Neha; euk;G #lhFe; jhfkhFk;

Mthd mUrpnahL rj;jp tpf;fy;

33
 mjl;bNa ,UkYld; Rthrk;

thyhf tapw;wpypiur;ryjprhu Njhrk;

kRu% kz;lhjy; khHfdj;jy;

Ntuhf Nkdp naq;Fkpf NtCjy;

tprghz;L mrhj;jankd;Nw tpsk;gyhNk.”

 Pallor of the skin
 Warmness of the blood vessels
 Excessive thirst
 Anorexia
 Vomiting
 Hic cough
 Cough
 Dyspnoea
 Flatulence
 Diarrhoea
 Pyrexia
 Anasarca
 Heaviness of the chest
 Very bad prognosis
3.3.3 jd;te;jpup itj;jpak;
(jd;te;jpup itj;jpak; ,uz;lhk; gFjp (ghz;L epjhdk;)
 thjg; ghz;L

“ Md fz; kyryq;fs; efq; fWg;ghFe;

jhfkh kq;fnkq;Fe; jbybgLif Nghy

kPdkha; eLf;fKz;lha; kire;jJH gyKz;lh

khd ePH thj ghz;L ntd;dNt tFf;fyhNk 07

 Blackness of the eyes, nail, urine and faecies

 Excessive thirst
 Body pain
 Tremor
 Tiredness
34
 gpj;jg; ghz;L

“ cw;wNjhH td;dNgjk; mNuhrf Kjuke;j

Kw;wpa khHG NehT %j;jpuk; nghd;dpd; td;dk;

ntw;wpNrH Gwq;fhy;iffz; tPq;Fly; ntSj;jy; NtHj;jy;

gw;wpa njhf;fpw; fha;jy; gapj;jpa ghz;L thNk.” 06

 Hatedness of food
 Anorexia
 Chest pain
 High coloured urine (gold colour)—
 Oedema in dorsum of the feet,hand and periorbital area
 Pallour of the skin
 Excessive sweet
 Warmness of the skin

 fgg; ghz;L
“ tFj;jpbw; rf;jpAz;lh kw;WNk aUrpAz;lh

kpFe;jtha;g; gpisg;GKz;lh tPf;fq;fs; ntSG;GKz;lhk;

efj;jpdpy; ntSg;GKz;lh tPf;fqfs; ntSg;GKz;lhk;

gFj;jpLQ; rpNyw;gdj;jpw; ghz;Lntd;Wiuf;fyhNk.” (8)

 Vomiting
 Anorexia
 Dyspnoea
 Anasarca
 Pallor of the skin and nail
 Diminished volume of pulse
 Kf;Fw;wg; ghz;L

“ ciuj;jpby; Gw;q;fhy; Nkw;ifnahspH Kff;fz;Z tPq;Fk;

epiuj;jLkpisg;Gr; rj;jpnaLf;Fk; khHgpdpy; typf;Fk;

Eiuj;jePH efq;fs; kQ;rsy;yJ fWg;G Nehf;Fe;

35
 jpiue;Jly;fLf;Fk; tpaHf;Fe;jpupNjhr ghz;Lntd;Nw (9)

 Pedal oedema
 oedema of arms,face and eyes
 Dyspnoea
 Vomiting
 Chest pain
 Frothy urine
 Black or yellow coloured nail
 body pain
 Excessive sweating

 gpj;jfgg; ghz;L kw;Wk; gpj;jthj ghz;L

“ vd;wpLk; gpj;jg; ghz;L tpjNdhL thjghz;L

nthd;wpbw; gpj;jthj ghz;L ntd;NwhjyhFk;

md;wpAk; gpj;jg; ghz;L tjNdhL rpNyw;k ghz;L

nrd;wpbw; gpj;jNrj;k ghz;Ltha;r; nrg;gyhnk (10)

 rd;dpthj ghz;L

“ nrg;gpa jpupNjhrj;jpd; nra;ifAz;lhf uj;je;

jg;gpa ruPuk; tPq;fr; rykyk; efq;fs; nghd;Ngh

ypg;gbr; re;epthj ghz;L tpdpay; gjhF

nkhg;GW kUe;jpw; wPuh jrhj;jpa nkd;dNthNj (11)

 Anasarca due to altered blood

 Yellow colouration of the feceis and nail
 High coloured urine
 Incurable
3.3.4 guuhrNrfuk;
 thjg; ghz;L

“ thjj;jp nyLj;j ghz;L tUq;Fzk; typFj; Jz;lhk;

jPJw;w Tly; eLq;FQ; NrHe;jpL tPf;f nka;g;Gg;

36
 NgJw;W kyryq;fs; efq;fSq; fWg;Gf; nfhs;Sk;

NrhJw;W tapW tpk;Kq; nfhz;bL kNuhrp fe;jhd;”

“ciuj;jpLk; fz;Z ehf;F Kjl;Lld; ruPue;jhDk;

Giuj;Jw epwNk nfl;Lg; nghupe;jpL kyq;flhDk;

tpiuj;jlq; Foyh ape;j nkypTfs; fz;l NghNj

ciuj;jdh thj ghz;nld WzHe;jpL KdptH jhNk”

“ ifAq; fhYe; fdj;Jise;J fz;Z KfKk; tapwijf;Fk;

nka;Ak; fdj;J ntSj;jpUf;Fk; ntz;zPh; Eiuaha;tapwpopAk;

IAkq; Nfhgpj; jpisg;Gz;lh gpd;dQ; nrWj;jq;F the;jpf;Fk;

nra;Ak; thj ghz;Lntdpj; njupe;j ngupNahH nrg;gpdNu”

 Pain
 Shivering
 Heaviness
 Pallour of the body
 Anasarca
 Blackish urine, fecies, nail
 Distended abdomen
 Anorexia
 Pallor of the eyes, tongue, lips, skin
 Pain in both extremities
 Swelling of eyes and face
 Frothy and watery stool
 Hatedness of food
 gpj;jg; ghz;L

“ gpj;jjj; jP nyLj;j ghz;L NgReh twl;rp Az;lhk;

kw;Wly; gRik ahfp kQ;rsp dpwK Kz;lhk;

cw;wpL%Hr;ir jhf nkhopnfLq; fz;flhKk;

Jw;wpL kow;rp thapw; JHehw;wk; Gspj;Njf; Fz;lhk;”

37
 “,UkNy apisg;G neQ;rp ypbg;gpld; Wug;G khfpg;

ngUfNt elf;Fk; NghJ NgRKw; lJNt ahFk;

ntUTwf; fpWfp Wf;F NkdpAk; ntSj;jijf;Fk;

ngUfpa gpj;j ghz;L thnkdg; NgrpdhNu

cjanka; aijj;Jf; iffh Nyha;e;Jld; Rue;J Nehtha;g;

GijaNt tPq;Fq; fz;Zk; NghjNt ntSf;FQ; NrhHthg;

gjfu kfpY kpQ;rpr; nrhwptjh arWgw;Wk;

tpjKW Fzq;fs; gpj;j ghz;nld tpsk;gpdNu”

 Dryness of the tongue
 Greenish yellow coloured skin
 Dizziness
 Thirst
 Dimness of vision
 Bad breath
 Water Brash
 Cough
 Giddiness
 Dyspnoea on excertion
 Pallor and oedema of the body
 Pain and weakness of the limbs
 Pallor of the eyes
 Tiredness
 Dirty scaly skin due to scaching Extremities

 rpNyw;gd ghz;L
“nka;Na ntspWk; tapwijf;Fk; tPq;Fk; Gwq;fhy;Gwq;iffsp

iffh NyhAq; fpWfpWf;Fk; fz;ZKfKk; gQrhFk;

Ja;a kheP uoha;e;JtpOe; njhz;il fre;J Jug;GkpFk;

INa ff;F kpf;Fzq;f swptha; Nrw;;g ghznldNt”

38
 “ NtHj;J ntUtpf;fz FspUk;ntr; nrdpwpUf;Fk; tpy;neQ;Rk;

MHf;FQ;JbNgh ypbf;FkJ itAk;gpj;jq;fye;JtUk;

jPHf;f kd;wp kwjpAz;lhe; jpw;wp ehTk; tOtOf;Fk;

ghHj;jh Slk;G tPf;fKwQ; Nrw;g ghz;L tpJ gfNu”

“fz;Z ehT KjLklk;Gkq; fUJ kyNkhH gpufhuk;

cz;Zq; fuKq; fhy;jhD KlNd ntSf;F Kfkjpw;

gz;Ze; jhf Kz;lhFk; grpaw;wpUf;Fk; ghHj;jpjid

kz;Ze; rpNyw;g ghz;LU ntd;nwOjpitj; jhHngupNahNu”

 Pallor of the face,eyes,tongue,extremities and lips

 Oedema of the dorsum of feet and hand
 Weakness of the both limbs
 Pallor of the faecies
 Giddiness
 Sweating
 Palpitation
 Tachycardia
 Loss of memory
 Loss of appetite
 Bitter taste in the throat
 Anasarca
 Excessive thirst

 rd;dpg; ghz;L

“ Xjpa thj gpj;j Nrw;gdq; Nfhgpj; Njhq;Fk;

CijA kpFe;J tpk;kp AjuKq; fhYk;tP;q;Fk;

Ngjkh apisf;Fk; tpf;f Ythe;jpAk; gpuikjhfk;

NfhijNa rd;dp ghj ghz;Ltpd; FzkpjhNk”

“ jd;Dj J}q;f Kfkijj;Jf; iffhNyha;e;J fpWfpWf;Fk;

NgZ krdQ;nrWj;J tpk;kpNahq;fhupj;J neQ;brupf;Fk;

39
 NrHjtpf;F ehtuSe; jhf Nkhfk; gpuikkhk;

NtNdNfsha; jpupNjh\j;njhe;jpj; Njhq;Fk; ngUk;ghL”

“td;dpAlD} ijiaaq; Nfhgpj; Njhq;F

kQ;rzpj;Nj apisg;Gkha; kaf;f khfpj;

Jd;dpUky; fz;Gifj;jy; if fhNyha;jy;

Juh;ngOjy; gpuikNahL Nrhfkhjy;

kd;Dq; Kk;kyePh; fz; ntSj;jy;

the;jp nfs;sy; tapW}jy; khNd Nfsha;

rd;dpAW ghz;LnrAq; Fzq;fnsd;W

rhw;wpdhH thflE}y; jd;id aha;e;Nj”

 Swelling of abdomen
 Lower extremities
 Dyspnoea
 Hic cogh
 Vomiting
 Delirium
 Weakness of the limbs
 Hatedness of food
 Nausea
 Heartburn
 Dryness of the tongue
 Excessive thirst
 Illusion
 Giddiness
 Faintness
 Dimness of vision
 Pallor of eyes, urine and faeces
 Swelling of abdomen

40
 kpUj;jpfh ghz;L

“ KfnkhL Gw;fhy; tPq;F Kl;Ll spisg;G Kz;lhk;

kpfT neQ;rpbf;Fk; kz;nz tpUk;gp nkd;NkYe;jpd;Dk;

jfTWk; tapW tpk;Kq; fpUkpA kyj;jpw; gw;Wk;

njhifgL Fzq;fs; kz;zhw; Nwhd;wpLk; ghz;LthNk”

 Oedema of face and dorsum of feet

 Breathlessness
 Palpitation
 Distended abdomen
 Worm infestation
 Excessive mud eating

NtnwhU tif 03
 Rughz;L

“ fhaKlk;gp nyyg; NghJq; fz;Ze; J}q;fpf; fpWfpwZk;

thA Klk;gpy; tplk; Nghyhk; thq;fpg; Grpf;f khl;lhJ

rhaq; fhy kpUkYWKjuk; tpk;Ke; jhfKWk;

gha ePUQ; RLkyKk; gr;nrd; wpUf;FQ; Rughz;Nl”

 fever
 drowsiness
 giddiness
 hatedness of food
 Evening cough
 distented abdomen
 Excessive thirst
 Hot micturation
 greenish stool

41
 uj;j ghz;L

“ Ruj;jpw; gpj;je; Njhd;wp AjpuNk nrhupe;J ff;Fk;

neupj;jpLk; Gut Kr;rp apbj;jpL nel;ilAz;lhk;

fuj;NjhL fhY NkhAq; fz;Kfk; Gija tPq;Fk;

,uj;jkhk; ghz;L nra;Aq; Fznkd tpak;gpdhNu”

“tha;ePH Row;wp neQ;nrupf;F kyKQ;ryKQ; rpte;jpLk;

Njdp Nghy kplwpiuAQ; rpy;nyd;wilf;F kpUfhJk;

CNd AUf;Fkq; fgk; tpO Nkhq;fhdpf;F Kjpuk;tpOk;

khNd fhYk; tapwijf;Fk; tFj;jh upuj;jghz;LNt’

 fever
 headache
 Haematemesis
 Weakness of the lower limbs
 Oedema of eyes and face
 Excessive salaivation
 Heartburn
 Redness of urine and faeces
 Tinnites
 Emaciation
 Nausea
 Melanoptysis
 Distended abdomen

 %yghz;L

“fhy; if Nahe;jly; fha;e;J ntSj;JfpH

rhy Ntngyd; whDq; Fiwe;jpLk;

#y Nkw;nfhz;LzT RUq;fpLk;

%y ghz;bd; Fzj;jpid nkhope;jdh;”.

 Weakness of the limbs

42
 Fever
 Pallor of the skin
 Fatigue
 decreased intake of food

3.3.5 kjiyNeha; kUj;Jtk;

“jpkpHj;jpLk; clynjq;Fk; NruNt tPf;fKz;lhk;
jkpHj;jpLk; tapWte;J js;spLk; kyk; tplhJ
fkHjpLk; ,ikkbAk; fz;tpop njupe;jplhJ
jpkpHe;jpLk; kUe;jd;Wk; jpl;nld Kf;Fk; jhNd
Kf;fpLk; %f;fpy; ePuhk; Kjpa ehtwz;L jhfk;
Jf;fpLk; Fly; ePNuw;wk; Ja;a ntz; gQ;R NghNy
gw;wpNa mfk; ntSj;J gue;J Nky;%r;Rz;lhk;
ke;jpu thiyg;ghz;L kuznkd;wwpa yhNk”

3.3.6 mDNghf itj;jpa Njt ufrpak; 06

 thjg; ghz;L
 Black or redness of the nails, eyes, urine, faeces
 tremer
 Constipation
 Headache
 Bodypain
 Flatulences
 anarsarca
 Pain in the sides of the thoracic, lower abdomen
 Loss of appetite

 gpj;jg; ghz;L
 Yellow coloured nails, eyes,urine, faeces
 Excssive thirst and sweat
 Desire to cold substances
 Bad breath
 Pungent taste
 Hallitosis

43
 Constipation
 Eructation
 Yellowish colouration of the body
 Chest pain
 Dyspnoea
 Giddiness

 fgg; ghz;L
 White colour of eyes, urine and faecies
 Laziness
 Tiredness
 Salty taste
 Sore throat
 Horropillation
 Vomiting
 Sneezing
 Giddiness
 Cough with expectoration
 Ejaculation of sperm

 Kf;Fw;wg;ghz;L
 The all symptoms of above classification occurs along with
 Dyspnoea
 Chest pain
 Obesity
 tiredness

 kpUj;jpfh ghz;L
 Due to excessive intake of mud ,rasam , and raktha thathu becomes weak and
result Pandu noi.
 Constipation
 Haematamesis
 Oedema of umbilicus, pedal, face, external genetalia
44
 tplg; ghz;L
 If above pandu’s are not treated properly
 Anorexia
 Thirst
 Warmness of the body
 Dyspnoea
 Diarrhoea
 Cough
 Vomiting
 Hic cough
 Tiredness of the chest
 Pyrexia
 Yellow or paleness of the skin
 It is incuarable

3.3.7 [Pt uf;rhkpHjk;

 thjg; ghz;L
 Pain all over the body
 Slightly darker of nails, urine an faeces
 Dull looking face
 Headache
 Constipation
 Loss of appetite
 Thirst
 Dull pain in the chest and lower abdomen

 gpj;jg; ghz;L
 Yellow or juicey green colour of blood vessels
 Fever
 Thirst
 Over sweating
 Dimnished vision
45
 Fainting
 Yellow colour of the body
 Pungent taste even at sleep
 pyrexia
 Coated tongue
 Eructation
 Bitter taste
 Constipation
 Giddiness and dyspnea

 fgg; ghz;L
 Pallor of the blood vesselse
 sour taste
 Cough
 Sore throat
 Sneezing
 Vomitting
 Syncope
 Dyspnoea
 Burning sensation

 jpupNjhrg; ghz;L
 It consists of the charecters of Vatha, Piththa, Kapha pandu associated with
anasarca and general debility

 kpUj;jpfh ghz;L
 Pervertion of appetide in the form of the geophagia.
 Derangement of Vatha, Piththa, Kapha
 Affects the digestive system
 Piththa thathu is mainly affected by the agni in the stomach, results dryness of the
rasathathu.
 Leads to improper formation of raththa thathu

46
 Swelling around the umbilicus, face, legs and genital organs , worms in the faeces,
cough with expectoration, with blood tinch

4.0 SIDDHA COMPLICATION

rpj;j cgj;jputq;fs;

4.1 ghz;L njhlH Neha; njhlHghf A+fpKdpapd; tpsf;fk;

“tpsk;gNt ghz;LKw;wp ,Uf;Fk; NghJ

kPwpNa gpj;jt];J jidg;G rpj;jhy;

Gsk;gNt kq;ifAld; GzHr;rp nra;jhy;

G+z;bLNk fhkhiy nad;Dk; Nuhk;”

4.2 gpj;j epjhdk;

“ Nfhy Kw FbnfhLf;Fk; ghz;LNuhfk;
Nfhgpj;J ehs; nrd;why; tUj;jk; nra;Ak;

ghz;Ltp;d; mrhj;jpa yl;rpaq;fs;.

4.3 khjt epjhdk;

 ePbj;;J njhlHtJk; kpf;f KjpHe;J NghdJkhd ghz;Lrpfpr;irf;F
trg;glhJ
 mtatq;fs; tPq;fpg;Ngha; vy;yhg;nghUSk; kQ;rshfj; Njhd;wpdhy; jPuhJ.
 ,Wfpa nrhw;g kyj;Jld; kQ;rs; ePuhfTk; fgj;Jld; $bajhfTk; mjprhuk;
cz;lhdhy; mrhj;jpak;
 mjpf jPj; jd;ik mile;J mtatq;fs; ntz;ikahfp the;jp %Hr;ir
ehtwl;rp cz;lhdy; mrhj;jpak;.
 ,uj;jk; nfl;L cly; Kw;Wk;; ntSj;jhy; jPuhJ.
 Njfj;jpy;> if> fhy;> jiy tPf;fk; cly; tw;wp ,isj;Jg; Nghdhy; Fjk;>
Mz;Fwp> gP[k; tPff
; k; ,Ue;jhy; jPuhJ.
 kpf;f ,isg;G kaf;f epiy fhzg;gl;lhy; jPuhJ
 mjprhuk;> Ruk; nfhz;l ghz;L jPuhJ.

4.4 ruNge;jpuH itj;jpa Kiwfs;

 tPf;fj;jpy; kQ;rs; epwk; fhzg;gl;lhy; Fzk; Vw;glhJ
 kyr;rpf;fNyh my;yJ gr;ir epwkhd mjprhuk; Vw;gl;lhy; mrhj;jpak;

47
 gytPdk;> the;jp> %Hr;ir> mjpf ehshd ghz;L Nuhfk; rpfpr;irf;F
trg;glhJ GjpjhdhYk; cly; eh twl;rp> ,uj;jf; Fiwtpdhy; cly;
ntSg;G KjypaitfSld; $ba NuhfpAk; FzkiltJ rpukk;.
 gw;fs;> efk;. fz; ,itfs; mjpfk; ntSj;jhYk; vy;yhtw;iwAk;
ntz;zpwkhfg; ghHj;jhYk; me;j Nuhfk; mrhj;jpakhFk;.
 iffs;> fhy;fs;>jiy Kjyhd ,lq;fspy; tPf;fk; Vw;gl;L ,isj;J if
fhy;fSk; ,isj;J tapW ngUj;Jk; cs;s ghz;L NuhfpiaAk;> Mz;Fwp>
njhil ,Lf;F Mfpa ,lq;fspy; tPf;fk;> mbf;fb kaf;fk;> mjprhuk;>
Ruk; Mfpad fz;L tUk; NuhfpiaAk; Fzg;gLj;JtJ mrhj;jpak; MFk;.

4.5 mfj;jpah; itj;jpaH gps;isj; jkpo;

 ghz;L Nuhfpf;F tPf;fk;> Nrhk;gy;> jhfk;> mNuhrfk;> the;jp> tpf;fy;> ,Uky;>
Ngjp vd;Dk; ,f;FwpFq;fs; cz;lhfp ve;jg; nghUisg;ghHj;jhYk; kQ;rs;
epwKz;lhjy; mrhj;jpak;.

4.6 Foe;ij Neha;fs; rpjk;gujhDg;gps;is

 Foe;ijfSf;F cz;lhFk; Ie;Jtifg; ghz;L Neha;fspy; thjghz;L>
gpj;j ghz;L ,uz;Lk; rhj;jpak;.
 rpNyj;Jkg;ghz;L> njhe;jg; ghz;L> uj;jg; ghz;L Mfpa %d;Wk; mrhj;jpak;.

4.7 fz;Zrhkpak;
 “ nrhy;Y gpj;jj;jpw; Nrhig Nrhigjdpy; thA njhe;jk;
ty;ytjpw; ghz;Ltd; ghz;by; - ey;y

tapw;Wf; fLg;G tsHfLg;gpw; rPjk;

gapypw; nfLjp nadg;gd;

ntg;Gg; gpzpajdpy; ntk; Nkfj;jhy; tUe;jpd;

jg;G kpif ePNu jhdpwq;fpd; - nrg;Gk;

fpuhzpapw ghz;by; fpsH ePH RUq;fpw;

gpuhzd; gpupankdg; NgR”

 “ ghz;L gpuNkfk; gd;thj #iy Fd;kk;

Ntz;lh raQ;rd;dp ntz;Nrhig – ePz;l

mjpePNu fhkhiy ahdgpzp jk;K

sjp rhukh fhjwp”

48
4.8 rjf ehb
 “ njhFj;jpl;l ePupopT Nkf#iy
RutPf;fQ; re;jp typNjhl khe;jk;

kpFe;jpl;l fpuhzp ajprhuk; thjk;

tplghfeljpud; ghz;L Nrhif fhkhiy

tFjjpl;l ngUk;ghL kQ;rs; NehT

tha;T uj;j gpj;jKld; gy NehTf;F

gFj;jpl;lapisg;GlNd Rthrk; tpf;fy;

gw;wpdhy; kuznkd;W gFj;Jr; nrhy;Ny”

ghz;L Nehapy; fgk; mjpfupj;jhy; Nrhig Njhd;Wk;. gpj;jk; NkYk;

mjpfupj;J kQ;rs; fhkhiy Neha; Vw;gLk;.

5.0 SIDDHA INVESTIGATION

gpzpawpKiwik
gpzpawpKiwik vd;gJ cliyg; gpzpj;jyha Nehiaj; njupe;J
nfhs;Sfpd;w xOf;fk; vdg;gLk;.

,J nghwpahywpjy;> Gydhywpjy;> tpdhTjy;> vd;Dk; tpjpfisAk;

mtw;iwj; Jizahfg; gw;wp xOFk; xOf;fq;fisAk; Fwpf;Fk;.

5.1 nghwpahywpjy;
Njhy; - if> fz;> eff;fz; ntSj;jy;
eh - nkd;ikahd gOg;G epwkhd gsgsg;ghd ehf;F.
fz; - nts;tpop ntSj;jy;
%f;F - ,ay;G
fhJ - ,ay;G
5.2 Gydhywpjy;
Rit - Ritapd;ik
ghu;it - kq;fpa ghHit
CW - Njhy; twl;rp
xyp - fhJ ,iur;ry;
kzk; - ,ay;G

49
 5.3 tpdhTjy;
Nehahspapd; ngaH > taJ> njhopy;> ,lk;> FLk;g #o;epiy FLk;g
tuyhW> Nehapd; fhyk;> Ke;ija tuyhW> fhy khWghLfs;> kUe;J
vLj;Jf;nfhz;ljw;fhd tuyhW kw;Wk; gof;f tof;fq;fs; Mfpatw;wpid
Nehahsp my;yJ ngw;Nwhuplk; Nfl;Lg;ngWjy;.

5.4 vz;tifj; NjHT

ghz;L Nehapy; vz;tifj; NjHT

gpzpia mwpAk; top kUj;Jt E}y; ty;NyhHfshy; vz;tifaha;
tFf;fg;gl;Ls;sJ.

“ ehbg;guprk; ehepwk; nkhoptpop

kyk; %j;jpukpit kUj;JtuhAjk;”

- Neha; ehly; Neha;Kjy; ehly; vd;gjdhYk;

“ehbahy; Kd;NdhH nrhd;d ew;Fwp Fzq;fshYk;

ePba tpopapdhYk; epd;w ehf;Fwpg;gpdhYk;

thba NkdpahYk; kynkhL ePupdhYk;

#ba tpahjp jd;idr; Rfk; ngw mwpe;J nrhy;Ny”

-mfj;jpaH

“ njhFf;fYw;W ml;ltpjg; guPl;ir jd;id

Jyf;fKWk; gz;bjNu njspthfg;

gFf;fupa ehbia eP gbj;Jg; ghU

gfHfpd;w thHj;ijiag; ghHehitg; ghU

tFf;fupa Njfnkdj; njhl;Lg; ghU

tskhd ruPuj;jpy; epwj;ijg; ghU

rfpf;fupa kyj;ijg; ghH ryj;ijg; ghU

rhHe;j tpopjidg; ghHj;J njsptha;f fhNz”

-mfj;jpaH itj;jpa ty;yhjp

50
 “ nka;f;Fwp epwe;njhdp tpopehtpUkyk; iff;Fwp”

vd;Dk; NjiuaH thf;fpdhYk; mwpayhk;.

5.4.1 ];guprk;
Njhy; twl;rp> nrhunrhug;Gf; fhZk;
5.4.2 eh
ghz;L Nehapy; eh ntSg;G> Ritapd;ik cz;lhFk;.
5.4.3 epwk;
cly;> fz; nts;tpop> eff;fz; ntSg;G cz;lhf;Fk;;.
5.4.4 nkhop
,ay;G
5.4.5 tpop
ghz;L Nehapy; fz; nts;tpop ntSj;jpUf;Fk;.
5.4.6 kyk;
kyf;fl;L> fopr;ry; Vw;gLk;.
5.4.7 %j;jpuk;( rpWePH)

epwk;> vil> kzk;> Eiu> vQ;ry; vd;gd mwpjy; mtrpak;.

 ePh;f;Fwp
 “ mUe;JkhwpujKk; mtpNuhjkjha;
m/fy; myHjy; mfhyT+d; jtpHe;jow;
Fw;wytUe;jp cwq;fp itfiw
Mbf;fyrj; jhtpNa fhJ nga;
njhU K$h;j;jf; fiyf; fl;gL ePupd;
epwf;Fwp nea;f;Fwp epUkpj;jy; flNd” (NjiuaH)

 “ te;j ePHf;fupvil kzk; Eiu vQ;rnyd;

iwe;jpaYstsit aiwFJ KiwNa
NjiuaH

ghz;L Nehapy; rpW ePH mstpy; FiwAk

51
  nea;f;Fwp
 “ epwf;Fwpf; Fiuj;j epUkhz ePupw;

rpwf;f ntz;nza;NahH rpWJsp eLtpj;

njd;Wwj; jpwe;njhsp Vfh jikj;jjp

dpd;wjptiy Nghk; newptpopawpAk;

nrd;wJ GfOQ; nra;jpia AzNu”

Neha; ehly; Neha;Kjy; ehly;

 “ muntd ePz;bd/Nj thjk;”

“ MopNghw; gutpd; m/Nj gpj;jk;

Kj;njd;W epw;fpd; nkhopt njd; fgNk”

NjiuaH
 “tpiuTld; fjpHNghy; ePz;L Ntw;Wikf; Fzq;fs; fz;lhy;

FUjpjhd; Fzknjd;Nd” NjiuaH

fjpH Nghy; gutpdhy; ghz;L Neha;.

5.4.8 ehb
 ehb eil

“ nfhz;blNt faNuhfp fhrNuhfp

Fwpg;ghfr; rpw;wpd;gk; nra;j NgHfs;

mz;blNt jupj;jpuHfs; tpUj;jh; ghyH

md;ghfj; jz;zPupy; %o;fpNdhHfs;

nfhz;blNt ,tHfsJ cWg;gpd; jhJ

$wNt KbahJ vtHf;Ff; fpl;Lk;

gz;blNt ,g;guPl;ir ahHjhd; fhz;ghH

guhguj;jpd; kfpikapJ ghU ghNu

Neha; ehly; Neha; Kjy; ehly;

52
 “nka;asT thjnkhd;W

Nky; gpj;Nkhuiuahk;

Iaq;fhnyd;Nw mwp”

-fz;Zrhkpak;

Iaehb : “jhdKs;s NrHj;Jke;jhdpsfpy; ntg;G

VdKWq; fhkhiy ghz;L Nrhig

Iathj ghz;L : “ fz;lhNah rpNyw;gdj;jpy; thj ehb

tpz;lhNy ,isg;gpUky; Nrhig ghz;L

Iagpj;jk; : “ ,lkhd Nrj;Jkj;jpy; gpj;j ehb

ntF RuKk; ehtwl;rp ghz;L Nuhfk;

gpj;j ehb : “ MNkjhd; mj;jpRuk; ghz;L Nrhif

Mokhd tplhr;RuKk; gpuNkfe;jhd;

NghNkjhd; fhkhiy gpj;j ntl;il

nghy;yhj ghz;LlNd rpte;j ePuhk;

ehNkjhd; nrhd;NdhNk gpj;jf; $W”

-mfj;jpaH ehb rhj];jpuk;

53
 MODERN ASPECT - INTRODUCTION

Blood is a connective tissue in fluid form. It is considered as the ‘fluid

of life’ because it carries oxygen from lungs to all parts of the body and carbon
dioxide from all parts of the body to lungs. It is known as ‘fluid of growth’
because it carries nutritive substances from digestive system and hormones from
endocrine gland to all the tissues. The blood is also called the ‘fluid of health’
because it protects the body against the diseases and gets rid of the waste
products and unwanted substances by transporting them to the excretory organs
like kidneys.

1. PHYSIOLOGY

PROPERTIES OF BLOOD

1. COLOUR

Blood is red in color. Arterial blood is scarlet red because it contains more
oxygen and venous blood is purple red because of more carbon dioxide.

2. VOLUME

Average volume of blood in a normal adult is 5 L. In a newborn baby, the

volume is 450 ml. It increases during growth and reaches 5 L at the time of
puberty. In females, it is slightly less and is about 4.5 L.

3. REACTION AND PH

Blood is slightly alkaline and its pH in normal condition is 7.4.

4. SPECIFIC GRAVITY

Specific gravity of total blood : 1.052 to1.061

Specific gravity of blood cells : 1.092 to 1.101

Specific gravity of plasma : 1.022 to 1.02

5. VISCOSITY

Blood is five times more viscous than water. It is mainly due to red blood
cells and plasma.

54
 COMPOSITION OF BLOOD

Blood is classified as a connective tissue and consists of two main components:

1. Plasma, which is a clear extracellular fluid

2. Formed elements, which are made up of the blood cells and platelets

The formed elements are so named because they are enclosed in a plasma
membrane and have a definite structure and shape. All formed elements are cells
except for the platelets, which are tiny fragments of bone marrow cells.

Formed elements are:

 Erythrocytes, also known as red blood cells (RBCs)

 Leukocytes, also known as white blood cells

(WBCs) Platelets

Leukocytes are further classified into two subcategories called

granulocytes which consist of neutrophils, eosinophils and basophils; and
agranulocytes which consist of lymphocytes and monocytes.

The formed elements can be separated from plasma by centrifuge, where

a blood sample is spun for a few minutes in a tube to separate its components
according to their densities. RBCs are denser than plasma, and so become packed
into the bottom of the tube to make up 45% of total volume. This volume is
known as the haematocrit. WBCs and platelets form a narrow cream-coloured
coat known as the buffy coat immediately above the RBCs. Finally, the plasma
makes up the top of the tube, which is a pale yellow colour and contains just
under 55% of the total volume.

Blood plasma
Blood plasma is a mixture of proteins, enzymes, nutrients, wastes, hormones
and gases. The specific composition and function of its components are as
follows.

55
 Proteins

These are the most abundant substance in plasma by weight and play a
part in a variety of roles including clotting, defense and transport. Collectively,
they serve several functions:

 They are an important reserve supply of amino acids for cell nutrition. Cells
called macrophages in the liver, gut, spleen, lungs and lymphatic tissue can break
down plasma proteins so as to release their amino acids. These amino acids are
used by other cells to synthesis new products.

 Plasma proteins also serve as carriers for other molecules. Many types of small
molecules bind to specific plasma proteins and are transported from the organs
that absorb these proteins to other tissues for utilization. The proteins also help
to keep the blood slightly basic at a stable pH. They do this by functioning as
weak bases themselves to bind excess H+ ions. By doing so, they remove excess
H+ from the blood which keeps it slightly basic.

 The plasma proteins interact in specific ways to cause the blood to coagulate,
which is part of the body’s response to injury to the blood vessels (also known
as vascular injury), and helps protect against the loss of blood and invasion by
foreign microorganisms and viruses.

 Plasma proteins govern the distribution of water between the blood and tissue
fluid by producing what is known as a colloid osmotic pressure.

FUNCTION OF BLOOD

1. NUTRITIVE FUNCTION
Nutritive substances like glucose, amino acid, lipids and vitamins
derived from digested food are absorbed from gastrointestinal tract and carried
by blood to different parts of the body for growth and production of energy.

56
2. RESPIRATORY FUNCTION

Transport of respiratory gases is done by blood. It carries oxygen from

alveoli of lungs to different tissues and carbon dioxide from tissues to alveoli.

3. EXCRETORY FUNCTION

Waste products formed in the tissues during various metallic activities

are removed by blood and carried to the excretory organs like kidney, skin, liver,
etc. for excretion.

4. TRANSPORT OF HORMONES AND ENZYMES

Hormones which are secreted by ductless glands are released directly

into the blood. The blood transports these hormones to their target organs/
tissues. Blood also transports enzyme.

5. REGULATION OF WATER BALANCE

Water content of the blood is freely interchangeable with interstitial fluid.

This helps in the regulation of water content of the body.

6. REGULATION OF ACID BASE BALANCE

Plasma proteins and hemoglobin act as buffers and help in the

regulation of acid -base balance.

7. REGULATION OF BODY TEMPERATURE

Because of the high specific heat of blood, it is responsible for

maintaining the thermoregulatory mechanism in the body, i.e. the balance
between heat loss and heat gain in the body.

8. STORAGE FUNCTION
Water and some important substances like proteins, glucose, sodium
and potassium are constantly required by the tissues. Blood serves as a
readymade source for these substances. And, these substances are taken from
blood during the condition like starvation, fluid loss, electrolyte loss, etc.
57
9. DEFENSIVE MECHANISM

Blood plays an important role in the defense of the body. The white
blood cells are responsible for this function. Neutrophils and monocytes engulf
the bacteria by phagocytosis. Lymphocytes are involved in development of
immunity. Eosinophils are responsible for detoxification, disintegration and
removal of foreign proteins.

10. REGULATION OF OSMOTIC PRESSURE

The plasma proteins play the major role in regulating the osmotic pressure of
tissue fluids.

RED BLOOD CELLS or ERYTHROCYTES

Red blood cells are the non-nucleated formed elements in the blood. Red
blood cells are known as erythrocytes. Red color of the red blood cell is due to
the presence of the coloring pigment called hemoglobin. RBCs are more in
number compared to the other two blood cells, namely white blood cells and
platelets.

MORPHOLOGY OF RED BLOOD CELLS

 NORMAL SHAPE

Normally, the RBCs are disc shaped and biconcave (dumbbell shaped).
Central portion is thinner and periphery is thicker. The biconcave contour of
RBCs has some mechanical and functional advantages.

 NORMAL SIZE

Diameter : 7.2µ (6.9 to 7.4µ)

Thickness : At the periphery it is thicker with 2.2µ and at the

center it is thinner with 1µ.
Shape : This difference in thickness is because of the
biconcave shape.
Surface area : 120sqµ
Volume : 85 to 90cu µ

58
  NORMAL STRUCTURE

RBC has a special type of cytoskeleton, which is made up of actin and spectrin.

PRODUCTION OF ERYTHROCYTES

Areas of the body that produce erythrocyte cells are

1. In the early few weeks of embryonic life – yolk sac

2. During the middle trimester of gestation – Liver, Spleen, Thymus and

Lymphnodes.
3. Later part of gestation and after birth - Red bone marrow

4. Up to the age of five – Red marrow of all the bones.

5. After the age of 5 and adult – Red marrow of proximal end of long bones and
flat bones such as ribs, vertebrae, pelvis, sternum and iliac bone.
Sometimes under conditions of exchanged stimuli, reticulo endothelial
system also takes up the embryonic function and yellow marrow shall be
transformed into the red marrow. Even in these bones, the marrow becomes less
productive as age increase

GENESIS OF RED BLOOD CORPUSCLES

In the bone marrow there are cells called Pluripotential Haemopoietic

Stem Cells (PHSC) from which all the cells in the circulating blood are derived.
The large portion of reproduced stem cells differentiates to form the other cells.
The early offspring still cannot be recognized as the different types of blood
cells, even though they have already become committed to a particular line of
cells and are called committed stem cells.
The different committed stem cells will produce colonies of specific
types of blood cells. There, a committed stem cell that produces colony –
forming unit blast (CFU-B) and then erethrocytes produced from these are called
colony forming unit – erythrocytes( CFU-E)
Growth and reproduction of the different stem cells are controlled by
multiple proteins are called Growth inducer. The another set of protein are called
differentiation inducers whose function is differentiation of the cells.
59
STAGE OF DIFFERENTIATION OF RED BLOOD
CORPUSCLES

Colony forming unit erythrocyte (CFU-E) [primordial stem multipotential]

Proerythroblast [First cell that belonging the RBC series – unipotential]

Basophil erythroblast [Begins synthesis of haemoglobin]

Poly chromatophil erythroblast [contains basophilic cytoplasm and haemoglobin]

Normoblast [with small nucleus and more haemoglobin- orthrochromic

erythroblast]

Reticulocytes [small amount of basophilic reticulum is present]

Erythrocytes [Matured red blood corpuscles.]

60
61
The stage of maturation of the RBC are given below

Haemocytoblast

Stage 1 Proerythroblast Vit B12

Stage 2 Early Normoblast Copper

Stage 3 Intermediate normoblast Vit.c.

Stage 4 Late normoblast Iron

Reticulocyte Thyroxin

Protein

Erythrocyte Hormone

STAGE OF MATURATION OF THE RBC

Stage 1- Pro erythroblast (Megaloblast)

This early cell is large (15-20) µ and contains no haemoglobin. The

cytoplasm is basophilic. The nucleus is about 12µ and occupies about three
quarters of the cell volume and the chromatin forms a fine stippled reticulam

Stage 2- Early Normoblast (Early erythroblast)

This cell is smaller than pro erythroblast and shows active mitosis. The
nucleoli disappeared and cytoplasm is basophilic.

62
 Stage 3- Intermediate Normoblast (Late erythroblast)

This cell is smaller (10- 15)µ and shows active mitosis. Haemoglobin
beings to appear and its eosinophilic staining give cytoplasm a polychromatic
appearance.

Stage4- Late Normoblast (Normoblast) Substances necessary for

the formation of erythrocytes corpuscles:

Mitosis has now ceased and the diameter of cell is 7- 10µ. The nucleus
is smaller and the condensed chromatin assumes a “cart wheel” appearance and
finally becomes deeply stained in a uniform manner. This appearance is called
pyknosis and is a stage in the degeneration of the nucleus, which breaks up and
finally disappears owing to the extrusion or lysis and a young RBC (reticulocyte)
is formed. The maximum level of haemoglobin is attained and the cytoplasm
gives eosinophilic reaction.

Maturation of erythroblasts thus involves a decrease in the size of the

cell, increased condensation and finally pyknosis of the nucleus. There is
accumulation of haemoglobin and a change in the staining reaction of the
cytoplasm from the basophilic to eosinophilic viz polychromatophil.

Substances necessary for the formation of erythrocytes

corpuscles:

Protein, Iron, Copper, Manganese, Vitamins (B12, C and Folic acid),

Internal secretions (Thyroxine), Hormones (erythropoietin, androgens and
thyroxine).
FUNCTIONS OF RED BLOOD CELLS

1. Transport of oxygen from the lungs to the Tissues

Hemoglobin in RBC combines with oxygen to form oxyhemoglobin. About
97% of oxygen is transported in blood in the form of oxyhemoglobin.

63
2. Transport of Carbon Dioxide from the tissues to the lungs

Hemoglobin combines with carbon dioxide and form

carbhemoglobin. About 30% of carbon dioxide is transported in this form.

RBCs contain a large amount of the carbonic anhydrase. This enzyme is

necessary for the formation of bicarbonate from water and carbon dioxide. Thus,
it helps to transport carbon dioxide in the form of bicarbonate from tissues to
lungs. About 63% of carbon dioxide is transported in this form.

3. Buffering action in Blood

Hemoglobin functions as a good buffer. By this action, it regulates the

hydrogen ion concentration and thereby plays a role in the maintenance of acid-
base balance

4. In blood group Determination

RBCs carry the blood group antigens like A antigen, B antigen and Rh
factor. This helps in determination of blood group and enables to prevent
reactions due to incompatible blood transfusion.

Life span and fate of red blood cells

Average life span of red blood cell is about 120 days. Daily 10% of red
blood cells, which are senile, get destroyed in normal young healthy adults. This
causes release about 0.6% of haemoglobin into the plasma. From this 0.9 to
1.5mg% bilirubin is formed.

Normal values of erythrocytes

Infants - 4to 4.5 million/cu.mm .
2-6 years - 4.5 million/cu.mm
6 -14 years - 4.5 to 4.8 million/cu.mm

Adult

Female - 4.0 to 5.0 million/cu.mm

Male - 5.0 to 5.5 million/cu.mm

64
 HEMOGLOBIN

Hemoglobin is the iron containing coloring matter of red blood cell. It is

a chromoprotein forming 95% of dry weight of RBC and 30% to 34% of wet
weight. Function of hemoglobin is to carry the respiratory gases, oxygen and
carbon dioxide. It acts as a buffer. Molecular weight of hemoglobin is 68,000.

NORMAL HEMOGLOBIN CONTENT

Average hemoglobin content in blood is 14 to 16 g/dL. However, the

value varies depending upon the age and sex of the individual.

AGE

 At birth Hb level : 25g/dl

 Infants : 13.5 – 19.5g/dl

 Up to 1 year : 11 -14 g/dl

 From puberty onwards : 14 to 16 g/dl

At the time of birth, hemoglobin content is very high because of increased

number of RBCs

SEX

In adult male : 14 – 18 g/dl

In adult female : 11.5- 15.5 g/dl

FUNCTIONS OF HEMOGLOBIN

 Transport of respiratory gases

1. Oxygen from the lungs to tissues

2. Carbon dioxide from tissues to lungs

 Buffer action

Hemoglobin acts as a buffer and plays an important role in acid- base balance.

65
 STRUCTURE OF HEMOGLOBIN

Hemoglobin is a conjugated protein. It consists of a protein

combined with an iron – containing pigment. The protein part is globin and the
iron- containing pigment is heme.

TYPES OF NORMAL HEMOGLOBIN

Hemoglobin is of two types:

1. Adult hemoglobin - HbA

2. Fetal hemoglobin – HbF

Metabolisum of Haemoglobin:

This section deals with three aspects of haemoglobin

I. Synthesis of haemoglobin

II. Catabolism of haemoglobin

III. Conversion of haemoglobin to bile pigments.

Synthesis of haemoglobin

Haemoglobin is haem + globin. In adults synthesis of haemoglobin

takes places in the red bone marrow from 3 sources namely, protoporphyrin,
Iron and globin. Certain co-factors are required to facilitate the synthesis.

1.Vitamin B 12 (extrinsic factor) 2. Intrinsic factor

3. Folic acid group of vitamin 4. Copper

Synthesis of haemoglobin and maturation of the erythrocytes proceeds

simultaneously. The immature erythrocytes contain free porphyrin. As the
cells mature, the porphyrin content decreases and is replaced by haemoglobin.
Thus the circulating red blood cells, which are rich in haemoglobin, contain
only traces of porphyrin.

66
Catabolism of haemoglobin:

Erythrocytes at the end of their life span of 120 days are broken
down. Simultaneously the haemoglobin is degraded. Daily about 8gms of
haemoglobin are broken down in the body and this corresponds to the
formation of about 300mg of bile pigments per day. The normal sites
of haemoglobin degradation are the reticulo endothelial cells of the
spleen, bone marrow and liver. The globin which is the protein portion
may be reutilized as such or may break down further into its constituent
amino acids and enter to the amino acid "pool" for reutilization. The
haem portion breaks down resulting in the formation of bile pigments.

Conversion of Haemoglobin to bile pigments:

Destruction of Destruction of
senescents RBC’s maturing erythroeid
cells

Haemoglobin

12-50%

Early labelled cells

Haem + globin
Turnover of Haem
+
Haeam products
Haem oxygenase

Biliverdin

Biliverdin reductase

Bilirubin (Unconjugated albumin bound)

UDP – Glucuronly transferase

Uptake of bilirubin (Liver)

67
 The haemoglobin released from the red cells is phagocytozed by
macrophages in the liver, spleen and bonemarrow. During the next few hours
to days, the macrophages release the haemoglobin back into the blood for
production of new red blood cells or to the liver and other tissues for storage
in the form of ferritin. The porphyrin portion of haemoglobin molecule is
converted by the macrophage through a series of stages into bile pigment
bilirubin, which is released into the blood and later secreted by the liver into
the bile.

Normal values of haemoglobin in different age groups

Mean Range g/dl

Cord 17.1
nn 13.7-20.5
7blood
days 18.8 14.6-23.0
20 days 15.9 11.3-20.5
45 days 12.7 9.5 -15.9
75 days 11.4 9.6 -13.2
120 11.9 9.9 -13.9
days
NORMAL VALUES

Packed cell Volume (Haematocrit value) – (P.C.V)

1 -13days : 54. 0 + /- 10.0%

14 -60days : 42.0 + /- 7.0%

3 months -10years :36.0 + /- 5.0%

11 -15years : 39.0 + /- 5.0%

Adult : 45 + /- 10.0%

68
Mean Corpuscular Volume (M.C.V)

1-13 days : 98 fl

14-60 days : 90 fl

3 month-10years : 80 fl

11-15 years : 82 fl

Adult : 82 to 92 fl

Mean Corpuscular Haemoglobin (M.C.H)

1-13 days : 38-33 picograms

14-60 days : 30 picograms

3 month-10years : 27 picograms

11-15 years : 28 picograms

Adult : 27 – 32 picograms

Mean corpuscular Haemoglobin Concentration (M.C.H.C)

1-13 days : 36 – 34 %

14-60 days : 33 %

3 month- 10 years : 34 %

11-15 years : 34 %

Adult : 32 – 36 %

69
 Reticulocytes

Cord blood : 5.0%

2 week : 1.0%

3 months : 1.0%

6months-6years : 1.0%

7-12 years : 1.0%

Adult : 1.6%

SYNTHESIS OF HEME

Heme is synthesized from succinyl-Co A and the glycine. The sequence

of events in synthesis of hemoglobin:
1. First step in heme systhesis takes place in the mitochondrian. Two molecules of
succinyl-Co A combines with two molecules of glycine and condense to form α
aminolevulinic acid (ALA) by ALA synthase.
2. ALA is transported to the cytoplasm. Two molecules of ALA combine to form
porphobilinogenin the presence of ALA dehydratase.

3. Porphobilinogen converted into urophobilinogen - I by urophobilinogen - I

synthase
4. Uroporphobilinogen - I is converted into uroporphobilinogen - III
byporphobilinogen - III cosynthase.
5. From uroporphobilinogen - III, a ring structure called coporphobilinogen - III is
formed by uroporphobilinogen decarboxylase.
6. Coprophobilinogen - III is transported back to the mitochondrion, where it is
oxidized to form protoporphyrinogen - IX by coproporphyrinogen oxidase.
7. Protoporphyrinogen - IX is converted into protoporphyrin - IX by
protoporphyrinogen oxidase.
8. Protoporphyrin - IX combines with iron to form heme in the presence of
ferrochelatase.

70
FORMATION OF GLOBIN

Polypeptide chains of globin are produced in the ribosomes. There are

four types of polypeptide chains namely, alpha, beta, gamma and delta chains.
Each of these chains differs from others by the amino acid sequence. Each globin
molecule is formed by the combination of 2 pairs of chains and each chain is
made of 141 to 146 amino acids. Adult hemoglobin contains two alpha chains
and two beta chains. Fetal hemoglobin contains two alpha chains and two
gamma chains.

CONFIGURATION

Each polypeptide chain combines with one heme molecule. Thus, after
the complete configuration, each hemoglobin molecule contains 4 polypeptide
chains and 4 heme molecules.

SUBSTANCES NECESSARY FOR HEMOGLOBIN

SYNTHESIS

Various materials are essential for the formation of hemoglobin in the RBC.

DESTRUCTION OF HEMOGLOBIN

After the lifespan of 120 days, the RBC is destroyed in the

reticuloendothelial system, particularly in spleen and the hemoglobin is released
into plasma. Soon, the hemoglobin is degraded in the reticuloendothelial cells
and split into globin and heme.

Globin is utilized for the resynthesis of hemoglobin. Heme is degraded

into iron and porphyrin. Iron is stored in the body as ferritin and hemosiderin,
which are reutilized into a green pigment called biliverdin. In human being, most
of the biliverdin is converted into a yellow pigment called bilirubin. Bilirubin
and biliverdin are together called bile pigments.

71
 3. PATHOLOGY OF ANEMIA

DEFINITION

Anaemia is a condition in which the number of red blood cells or their

oxygen- carrying capacity is insufficient to meet physiologic needs, which vary
by age, sex, altitude, smoking, and pregnancy status.

Iron deficiency is thought to be the most common cause of anaemia

globally, although other conditions, such as folate, vitamin B12 and vitamin A
deficiencies, chronic inflammation, parasitic infections, and inherited disorders
can all cause anaemia.

Anemia is the blood disorder, characterized by the reduction in :

1. Red blood cell count (RBC)

2. Hemoglobin content

3. Packed cell volume(PCV)

Grading of Anemia

WHO grades anemia according to hemoglobin level as follows,

Hb between 10 gm and cut off point for age : Mild

Hb between 7 to 10 gm : Moderate

Hb under 7 gm : Sever

WHO Criteria for diagnosis of Anemia

Children 6 months to 6 year : less than 11 g/dl

11 hildren 6 years to 14 year : less than 12 g/dl

IAP Text book of Paediatrics

72
4. PATHOGENESIS - Etiology of Anemia

Causes vary with age and anemia may be multifactorial

a. New born

History should include that for maternal infections, collagen vascular

diseases, prematurity, blood loss, jaundice(hemolysis due to ABO or Rh
incompatibility, G6PD deficiency, sepsis) and presents of hemangiomas or
cephalhematoma.

b. Young infants (3 months to 18 months)

In infants may have physiological anemia at 2- 3 months of age. Delayed

or inadequate weaning with predominantly milk- based diet results in poor iron
intake, leading to nutritional iron deficiency, usually occurring at 6 months to 2
yrs of age; other causes include chronic diarrhea or cow milk allergy.
Megaloblastic anemia may be nutritional, due to use of goat milk in infants and
a vegetarian diet in older children.

c. Older babies and children

1. Common causes

a. Malnutrition and iron deficiency

b. Infections

c. Nephritis, Nephrosis

d. Ankylostomiasis

2. Less common causes

a. Leukemia

b. Inherited defects pf RBC, haemoglobinopathies or congenital spherocytosis

c. Bleeding disorders like haemophilias, thrombocytopenic purpura and

petechial bleeding
73
 d. Rare causes – aplastic anemia and pernicious anemia
ETIO- PATHOGENISIS

1. Anemia due to defects in haemoglobin synthesis

When there is deficiency of Iron, Vitamin B12, Vitamin C, Folic acid,

Pyridoxine, Thyroxine, Proteins and Copper, there is decreased haemoglobin
synthesis

2. Anemia due to immaturation of red blood cells

In megaloblastic anemia large nucleated red blood cells are seen in the red
marrow of the bones. This immaturation is due to non- availability of Vitamin B
12, Folic acid.

3. Anemia due to red blood cell defects

The life span of matured red blood cells is about 120 days. Sometimes they
may die within their usual lifetime. This leads to anemia.

PATHOPHYSIOLOGY OF ANEMIA

Subnormal level of hemoglobincauses lowered oxygen carrying capacity

of the blood which leads to hypoxia in organs.
 Increased release of oxygen from hemoglobin

 Increased blood flow to tissues

 Maintenance of the blood volume

 Redistribution of blood flow to maintain the cerebral blood supply

SYMPTOMS AND SIGNS OF ANEMIA:

Symptoms:

Lassitude, easy fatiguability, breathlessness on exertion, palpitation,

tinnitus, throbbing in head and ears, generalized muscular weakness,
dizziness, headache, hair loss, insomnia, angina, dimness of vision,
paraesthesia in fingers and toes.
74
 Signs

Pallor (Pale skin, mucosal linings and nail beds) Cheilosis,

Koilonychia, Systolic flow murmurs, Oedema, Cardiac dilatation and
tachycardia.

CLASSIFICATION OF ANEMIA

Anemia is classified by two methods:

1. Morphological classification

2. Etiological classification

MORPHOLOGICAL CLASSIFICATION

Morphological classification depends upon the size and color of RBC.

Size is determined by mean corpuscular volume (MCV). Color is determined by
mean corpuscular hemoglobin concentration (MCHC). By this method anemia
is classified into four types.

1. Normocytic Normochromic Anemia

2. Macrocytic Normochromic Anemia

3. Macrocytic Hypochromic Anemia

4. Microcytic Hypochromic anemia

1. Normocytic Normochromic Anemia

Size and color of RBCs re normal. But the number of

RBC is less. Post-hemorrhage - early stage
- Hemolytic anemia

- IDA - early stage

- Systemic diseases like endocrinal, renal and hepatic diseases

- Bone marrow disorders like hypoplastic anemia, myeloinfiltration,

dyserythropoiesis, myelodysplasia and masked megaloblastosis.

75
2. Macrocytic Normochromic Anemia

RBCs are larger in size with normal color, RBC count is less. Folate and Vitamin
B12 deficiency, hypothyroidism.

3. Macrocytic Hypochromic Anemia

RBCs are larger in size. MCHC is less, so the cells are pale Combined deficiency
of Iron and folate or Vitamin B12
4. Microcytic Hypochromic Anemia

RBCs are smaller in size with less colour.

Iron deficiency anemia

Haemoglobinopatheis
Haemolytic anemia

Anemia

Macrocytic Normocytic Microcytic

anemia anemia anemia
(MCV>100) (80<MCV<100) (MCV<80)

High Low
Reticulocyte Reticulocyte
Count Count

76
 ETIOLOGICAL CLASSIFICATION

On the basis of etiology anemia is divided into five types

1. Hemorrhagic anemia

2. Hemolytic anemia

3. Nutrition deficiency anemia

4. Aplastic anemia

5. Anemia of chronic diseases

CLINICAL FEATURES OF ANEMIA

 The hemoglobin level at which symptoms of anemia appear, depends on the rate
of development of the anemia. Symptoms occur at higher hemoglobin levels if
anemia develops rapidly, as with hemorrhage.

 The most common and earliest symptoms include lassitude, and easily
fatigability. Alternatively, children may have anorexia, irritability and poor
school performance.

 Dyspnea on exertion, tachycardia and palpitations indicate severe anemia.

 Other symptoms include dizziness, headache, tinnitus, lack of concentration and

drowsiness and with severe anemia, clouding of consciousness.

 The most prominent and characteristic sign is pallor, detected most reliably in
nail beds, oral mucous membranes and conjunctivae.

 Observing palmar creases and skin is insufficient as the skin creases in children
lack pigmentation.

 Facial pallor varies with skin pigmentation and presence of edema.

77
 A mid-systolic “flow” murmur, chiefly in the pulmonary area, is appreciated
when the degree of anemia increases, reflecting increased blood flow across
heart valves. Systolic bruits and postural hypotension may be noted with
moderate to severe anemia.

Severe anemia is characterized by a high output state with an elevated

pulse pressure and a “collapsing” pulse. Anemia may participate heart failure
even with a normal cardiovascular system.

IRON

The total content of iron in an adult body is 3- 5 g. About 70% of this

occurs in the erythrocytes of blood as a constituent of hemoglobin. At least 5%
of body iron is present in myoglobin of muscle. Heme is the most constituent of
several proteins/enzymes (hemoproteins) - hemoglobin, myoglobin,
cytochrome, xanthine oxidase, catalase, tryptophan pyrrolase, peroxidase.

Functions of iron in the body

1. Iron mainly exerts its functions through the compounds in which it is present.
Hemoglobin and myoglobin are required for the transport of o2 and co2.
2. Cytochromes and certain non- heme proteins are necessary for electron transport
chain and oxidative phosphorylation.
3. Peroxidase, the lysosomal enzyme, is required for phagocytosis and killing of
bacteria by neutrophills.
4. Iron is associated with effective immunocompetence of the body.

Daily Iron requirement in different age groups:

 Pregnant and lactating females – 40mg/day

 Females 11 years to 30 years – 18mg/day

 Adults males - 10mg/day

 Males 11 years to 17 years – 12mg/day

78
 Upto 10 years (M/F) - 10mg/day

 Full term infants - 1mg/kg/day from 4 months of age

 LBW babies - 2/mg/kg/day from 2 months of age

 Babies 1000to 1500 grams – 3mg/kg/day from 2 months of age

 Less than grams - 4mg/kg/day from 2 months of age

IRON SOURCES
Rich sources
 Muscle meat

 Organ meat (liver, heart, kidney)

 Beef liver
Good sources
 Greens
 Leafy vegetables
 Nuts

 Cereals

 Wheat germs

 Fish

 Shellfish

 Poultry

 Egg

 Iron fortified cereals and foods

 Apples and dry fruits

 Jaggery

 Yeast

 Molasses

 Oysters
79
 Poor sources

 Wheat

 Polished rice

 Milk

IRON METABOLISM

Absorption, transport and storage

Iron is mainly absorbed in the stomach and duodenum. In normal people,

about 10% of dietary iron is usually absorbed. However, in iron deficient
individuals and growing children, a much higher proportion of dietary iron is
absorbed to meet the increased body demands.
Iron is mostly found in the foods in ferric form (fe3+), bound to proteins
or organic acids. In the acid medium provided by gastric HCL, the fe3+ is
released from foods. Reducing substances such as ascorbic acid(vitamin C) and
cysteine convert ferric iron(Fe3+) to ferrous form(Fe2+). Iron in the ferrous form
is soluble and readily absorbed.
Factors affecting iron absorption

1. Acidity, ascorbic acid, alcohol, fructose and cysteine promote iron absorption.

2. In iron deficiency anemia, iron absorption is increased to 2-10 times that

of normal
3. Small peptides and amino acids favour iron uptake.

4. Phytate (found in cereals) and oxalate (found in vegetables) interfere with

iron absorption.
5. A diet with high phosphate content decreases iron absorption while low
phosphate promotes.
6. Impaired absorption of iron is observed in malabsorption syndromes such
as steatorrhea.
7. In patients with partial or total surgical removal of stomach and/or intestine,
iron absorption is severely impaired.

80
Iron in mucosal cells

The iron (Fe2+) entering the mucosal cells by absorption is oxidized to ferric
form (Fe3+) by the enzyme ferroxidase. Fe3+ then combines with apoferritin to
form ferritin which is the temporary storage form of iron. From the mucosal
cells, iron may enter the blood stream (which mainly depends on the body needs)
or lost when the cells are desquamated.

Transport of iron in the plasma

The ironliberated from the ferritin of mucosal cells enters the plasma in
ferrous state. Here, it is oxidized to ferric form by a copper-containing protein,
ceruloplasmin which possesses ferroxidase activity. Another cuproprotein
ferroxidase 2 also helps for the conversion of Fe2+ to Fe3+.

Ferric iron then binds with a specific iron-binding protein, namely

transferring or siderophilin (a glycoprotein with mol.wt.90,000). Each
transferring molecule can bind with two atoms of ferric iron (Fe3+). The plasma
transferring (concentration 250mg/dl) can bind with 400mg of iron/dl plasma.
This is known as total iron binding capacity (TIBC) of plasma.

Storage of iron

Iron is stored in liver, spleen and bone marrow in the form of ferritin. In
the mucosal cells, ferritin is the temporary storage form of iron. A molecule of
apoferritin(mol.wt.500,000) can combine with 4,000 atoms of iron. The
maximum iron content of ferritin on weight basis is around 25%.

Hemosiderin

Hemosiderin is another iron storage protein which can hold about 35%
of iron by weight. Hemosiderin accumulates in the body(spleen, liver) when
the supply of iron is in excess of body demands.

Iron is a one-way substance

Iron metabolism is unique as it operates in a closed system. It is very

efficiently utilized and reutilized by the body. Further, iron losses from the body

81
are minimal which may occur through bile, sweat, hair loss etc. Iron is not
excreted into urine. Thus, iron
differs from the vitamins or other organic and inorganic substances which are
either inactivated or excreted during the course of metabolic function. Hence,
iron is appropriately regarded as a one-way substance.

Iron entry into the body is controlled at the absorption level, depending
on the body needs. Thus the periodical blood loss in menstruating women
increases its requirements. Increased iron demands are also observed in
pregnancy, lactation, and in growing children.

IRON DEFICIENCY ANEMIA

Iron deficiency anemia occurs when the decrease in total iron body
content is severe enough to diminish erythropoiesis and cause anemia. The
numbers are staggering ; 2 billion – over 30% of the world‟s population – are
anemic, many due to iron deficiency. The major factors which influence its
prevalence includes poor socio-economic status, low dietary intake, poor
accessibility to healthcare facilities and worm infestation in the population.

Iron requirements during childhood

Understanding of iron requirements, intakes and bioavailability is

essential to explain the vulnerability of some individuals to develop iron
deficiency anemia.

The iron released from the senescent, red cells during the first 8- 12 weeks
of life(a period of quiescent erythropoiesis) is stored in the body and helps to
maintain erythropoiesis upto 4-6 months in a normal term infant and upto 2-3
months in low birth weight infant. Normal infants at birth have about 75 mg of
iron per kg body weight, two thirds of which is present in red blood cells. Infants
and children should continue to absorb 0.8 to 1.0 mg of iron daily to reach the
adult body stores of 4-5 gms.

Normal body losses of iron are about 20µg/kg/day and most of these losses

82
 occur by the shedding of cells from intestinal mucosa. These losses are small
and are relatively
constant but may increase many folds in the presence of diarrhea,
dysentery, and parasitic infections.
Certain factors protect infants from becoming iron deficient in first few
months of life. These includes
 Preferential delivery of iron to the fetus during the pregnancy particularly during
last three months of gestation
 Placental transform to the newborn immediately after birth when the cord is
allowed to pulsate before being clamped.
 Exclusive breast feeding for first four to six months of life, due to better
bioavilability of iron from the breast milk.

Structures of the red corpuscles in IDA

In iron deficiency anemia, the red blood corpuscles are decreased or normal
in the number and hemoglobin content of the red blood corpuscles is reduced. In
the smear, the red cells appear pale with a large central pale area and many of
the red blood cells appear to be smaller than the normal. This type of anemia is
called “hypochromic and microcytic anemia”

Etiology – Iron deficiency anaemia

The etiology varies with the age, sex and country of residence of the patient

1. Increased physiological requirement

Rapid growth- infants and pre-adolescence
Menstruation

Pregnancy

2. Decreased iron stores

Preterms

Small for dates

Twins

83
3. Decreased iron assimilations

Iron poor diet

Iron malabsorption
Sprue
Pica

GITsurgery
Chronic diarrhea
Delayed weaning
Malnutrition

4. Blood loss

Gastro intestinal bleeding

Milk induced enteropathy

Peptic ulcer disease

Inflammatory bowel disease

Drugs- salicylates
Hook worm infestation
Fetal Maternal transfusion
Iatrogenic Bleeding diasthesis
Repeated venous sampling

5. Increased demands

Prematurity

Low birth weight Recovery

from PEM Adolescence

 Iron poor diet

 Dietary inadequacy is present in more than 80 % of cases especially in the

poorer groups. This is still encountered in privileged societies under the
following circumstances.
84
 Infants are also at high risk because the diet predominantly milk contains very
small amounts of iron. Human milk provides only about 0.3mg / litre of iron.
 Premature babies have only lesser amount of storage iron in the liver as well
as body
 Children especially during the early years of life have a need for dietary iron
to accommodate growth and expansion of the blood volume.

 Iron malabsorption

 Iron malabsorption is an unusual cause of iron deficiency where malnutrition

is rampant however both histologic and functional abnormalities of the
intestine are common. Defective iron absorption is caused by non- tropical
sprue.
 Partial or total gastrectomy impairs iron absorption caused by reduction in
gastric acidity and acceleration of the food through the upper portion of the
small bowel. The absorption of both haem iron and non-haem is defective.
 Pica or the habitual ingestion of non-food substances is common in children
and pregnant women. It markedly inhibit iron absorption.
 Pancreatic enzymes may contribute to the high incidence of iron deficiency
in patients with cystic fibrosis.

 Gastro intestinal bleeding

 Hookworm infestation (Ankylostomiasis) is the most important cause of

intestinal blood loss worldwide. The parasites Ankylostoma duodenale and
Nectar americanus attach to the proximal portion of the small intestine
and suck blood from submucosal vessels. The amount of blood lost is a
function of the hookworm load, which in turn is proportional to the number
of ova in the stool. Each worm has been in the intestine for months or years,
draws, 0.2-0.5 ml of blood per day. It has been estimated that the loss of
hemoglobin for every twelve worms may be one percent. Fecal ova counts in
excess of 5000/g are regularly associated with iron loss of more than 3 to 4
mg/day and a high incidence of iron deficiency anemia.
 Milk induced enteropathy associated with occult Gastrointestinal bleeding
has been implicated as the cause of iron deficiency in some infants.
85
 During the first year of life, meckel diverticulum is a well- recognized cause
of asymptomatic bleeding in adult men and postmenopausal women, occult
bleeding from the gastrointestinal tract is the most common cause of iron
deficiency.
 Gastrointestinal bleeding also is prevalent among iron deficiency infants and
children. Characteristically gastro intestinal bleeding is occult and
unsuspected.
 Peptic ulcer disease is a well – documented cause of occult blood loss.

 Crohn‟s disease and ulcerativecolitis also are commonly associated with iron
deficiency.
 Corticosteroids, Indomethacin and other non- steroidal anti-inflammatory
agents may also induce gastrointestinal tract bleeding.

Pathogenesis

Iron deficiency anemia develops when iron supply to the bone

marrow is insufficient for the erythropoiesis.
It has been stated that the body is normally in a state of positive iron
balance. When a negative iron balance occurs due to either blood loss, increased
requirements or impaired absorption, the deficit is made good by iron mobilized
from the tissues and an adequate supply of iron for haemoglobin formation is
maintained. It is only when the tissue stores are exhausted that the supply of iron
to the marrow for haemoglobin synthesis becomes inadequate and hypochromic
anemia develops. Thus iron deficiency may be regarded as developing two
stages.

 The progressive depletion and cumulative exhaustion of the available tissue

iron stores
 Iron deficiency state, which may be divided into three distinct stage of severity.

86
 TABLE - 02
Stage Manifestation

Early stage Storage iron depletion

Second stage Iron limited erythropoiesis
Third stage Iron deficiency anemia

Stages of iron deficiency anemia

1. Storage of iron Depletion

Iron reserve is small or absent and is characterized by reduced serum ferritin or

reduced iron concentration in marrow and liver tissue. Haemoglobin and serum
iron, Transferritin concentration and saturation are within normalimits.

2. Iron limited Erythropoiesis

Haemoglobin(Hb) may still be normal but serum iron is low and TIBC
increased with a low serum ferritin and raised free erythrocyte
protoporphyrin(FEP)
3. Iron deficiency anemia
The flow of iron to erythoid marrow is impaired to cause reduction in
haemoglobin concentration with a progressive microcytic hypochromic anemia
associated with reduced serum iron, transferring saturation and serum ferritin
level.

Role of iron deficiency anemia in various systems

Cardiovascular system
Dyspnoea and palpitation are common symtoms while on exertion but in
very severe anemia the patient may get cardiac failure and there may br dyspnoea
at rest. Haemic murmurs are commonlyheard in anemic patients. The murmurs
are most often mild systolic murmurs heard at the mitral area.
Systolic bruits over the carotid arteries in the neck are sometimes present
in anemia usually they are bilateral and occur in the absence of an aortic systolic
bruit and disappear following correction of the anemia. Jugular venous pressure
increase in severe anemia due to high pulse pressure with a capillary pulsation.
87
 Oedema of the legs occasionally occurs in ambulant patient with severe anemia
as the result of venous capillary pressure on exertion and increased capillary
permeability.

Central nervous system

Symptoms include faintness, giddiness, headache, roaring in the ears,

tinnitus, spots before the eyes, lack of concentration, drowsiness and with severe
anemia clouding of consciousness, numbness and sometimes tingling of the
hands and feet.

Productive system

Menstrual disturbances are commonly associated with anemia

Renal system

Slight proteinuria may be present with severe anemia. Anemia may

further reduce renal function at which nitrogen retention develops; correction of
anemia in such patient is usually followed by a fall in blood urea.

Gastro intestinal system

Anorexia is the commonest symptom, nausea, flatulence and
constipation may also occur. Slight to moderate smooth hepatomegaly is
common in severe anemia and
when congestive cardiac failure develops. The liver may become tender. In
certain cases of iron deficiency anemia spleen may be enlarged.
Pyrexia

Mild pyrexia may occur with severe anemia but marked fever is due to either
the causative disorder or due to some complicating factor.

Signs

 Pallor of skin, mucous membrane, palms, nailed and conjunctiva

 Koilonychia

 Tachycardia

88
 Smooth, pale, glossy palate

 High volume pulse

 Systolic murmurs

 Cardiomegaly

 Splenomegaly in rare cases.

Symptoms

 Weakness

 Fatigue

 Exercise intolerance

 Loss of appetite

 Irritability

 Lack of concentration

 Desire to ingest unusual substances like ice or dirt

 Giddiness

 Insomnia

 Constipation

 Breathlessness on exertion
 Dimness of vision

 Tinnitus
 Anginal pain

 Palpitation

 Parasthesia in fingers and toes

 Abdominal distension

89
 Complication of iron deficiency anemia

 In patients with heart disease severe anemia may precipitate angina pectoris or
congestive heart failure
 Infections are more common in Iron deficiency anemia, especially those of
respiratory, gastrointestinal and urinary tracts.

Investigation required for iron deficiency anemia

1. Blood investigation

 Total red blood cell count

 Differential count

 Erythrocyte sedimentation rate

 Mean corpuscular volume

 Mean corpuscular hemoglobin concentration

 Packed cell volume

 Peripheral blood smear

 Red cell survival

 Serum iron

 Serum ferritin concentration

 Serum protein

 Serum creatinine.

2. Urine investigation

 Urine sugar

 Albumin

 Deposits
 Red blood cells

 Pus cells
90
3. Stool investigation

 Occult blood

 Organisms

 Ova

 Cyst

 Red blood cells

 Pus cells

4. Special investigations occasionally required

 X- ray barium meal, X-ray barium enema, X-ray Chest

 Endoscopy, Colonoscopy, Sigmoidoscopy, Gastroduodenoscopy

 Isotope studies

 Skeletal survey for multiple myeloma and secondary deposits

 Bone marrow examination

 Liver function test

 Jejunal biopsy, urography, selective angiography

 Ultrasonography

DIFFERENTIAL DIAGNOSIS

1. Anemia of infection

2. Pyridoxine (vit B6) deficiency anemia

3. Haemoglobinopathies

4. Sideroblastic anemia

5. Anemia of lead poisoning

91
 DIAGNOSIS

Following criteria are essential to diagnose Iron deficiency

anemia

 History of inadequate intake of dietary iron and blood loss if any.

 Easy fatiguability, pallor, pica, koilonychias, smooth tongue, cheilosis, and
dysphagia associated with general comsiderations.
 Hypochromic and microcytic structure of red blood cells

 Low serum iron, increased total iron binding capacity.

 Bone marrow hemosiderin absent

 Blood loss usually occult

 Platelet count is either normal or raised

 Hemoglobin estimation variably reduced

 Reduced mean cell volume

 Erythrocyte count may be normal or reduced

 Serum ferritin level is reduced

MANAGEMENT

Management of IDA is considered by three methods

1. Correction of anemic state

2. Replenishment of iron stores

3. Elimination of the cause

PROPHYLAXIS

The main principles in the prevention of nutritional Iron deficiency anemia are,

1. The regular consumption of a well balanced diet containing an adequate

quantity of iron
2. The periodic administration of iron as drug during increased physiological
92
 needs such as rapid growth during infancy and preadolescence, pregnancy,
lactation and menstruation.
3. Maintenance of a normal hemoglobin level in the mother for the prevention of
iron deficiency anemia in infants. Premature and unduly small infants should
be given prophylactic iron as a routine therapy. Iron rich sources should be
added in the infants diet from the third or fourth month and thereafter be
progressively increased.

PREVENTION OF IDEA

The basic approaches to the prevention of IDA include

1. Protection and promotion of breast- feeding for as long as possible along with
timely weaning is effective in preventing IDA Low birth weight infants need
iron supplementation from the age of 2 months.
2. Dietary modification and consumption of larger amounts of habitual foods
increases total iron consumption by 25- 30 percent. Processes like germination,
consumption and green leafy vegetables would be additional long-term
methods for prevention of IDA.
3. Periodic deworming with anti-helminthic drugs for hookworm infestation and
schistosomiasis should be considered in endemic areas.
4. Supplementation with medicinal iron is considered necessary to reduce the
extent of anemia in developing countries.
5. Food and salt fortification with iron are evolving rapidly and would be one of
the most effective ways to control IDA. Salt fortification gives an iron content
of 1 mg per gram of salt in the preparation.

DIET - Haem iron sources

 Muscle meat (red more than white)

 Organ meat(e.g Liver)

 Fish and shellfish

 Poultry

93
 Non-haem iron sources

 Oatmeal

 Nuts

 Pulses

 Dried fruit

 Whole meat
 Bread, eggs

 Green leafy vegetables

 Iron fortified cereal foods

 Jaggery and yeast

 Foods rich in vitamin C enhance iron absorption.

Self care procedures for Iron deficiency anemia

1. Eat more foods that are good sources of iron

2. Concentrate on green leafy vegetables, red meat, beef liver, poultry, fish,
wheat germ, oysters, dried fruit, and fortified cereals
3. Foods high in vitamin C like citrus fruits, tomatoes and strawberries help the
body absorbing iron from food
4. Red meat not only supplies a good amount of iron, it also increases
absorption of iron from other food sources
5. Take an iron supplement

6. Increased dietary fibre to prevent constipation

7. Avoid aspirin and products with aspirin

8. Eat fresh uncooked fruits and vegetables often. Don‟t overcook food that
destroys folic acid.

94
EVALUATION OF DISSERTATION TOPICS

 MATERIAL AND METHODS

 DIAGNOSTIC METHODOLOGY
 OBSERVATION AND INFERENCE

 MATERIALS
 The clinical study and Paandu was carrieded in the out patient in post graduate
department of Noinadal at Government Siddha Medical College and Hospital
Palayamkottai, Thirunelvely.
 40 cases with clinical science and symptoms of Paandu both sex of all diferent
ages were studied under the guidance of faculties of post graduate department.

 Selection of patients
 The clinical study was done in cases, out of that 40 cases were selected on the
basis of clinical symptoms indicated in the Siddha text.

 Selection criteria
 Inclusion criteria
 Age - 40 years to 65 years
 Gender - Male and Female
 Haemoglobin - below 10g/dl
 Total RBC count - below 4.0 million/ mm3
 PCV - below 30%
 MCV - below 82 fl
 MCH - below 27 pg
 MCHC - below 32%
 Peripheral smear - Result show anaemia
 Patients who co-operate for investigation whenever necessary.

95
 Exclution criteria
 Age - below 39 years
 Age – above 65 years

 Investigation required

 Blood
 White Blood Count
 Differential count
 Red Blood Count
 Haemoglobin
 Pcak Cell Volume
 Mean Corpuscular Volume
 Mean corpuscular Hemoglobin
 Mean Corpuscular Haemoglobin Concentration
 Peripheral smear
 Blood grouping
 Erythrocyte Sedimentation Rate
 Blood sugar
 Blood urea
 Serum Cholesterol

 Urine
 Albumin
 Sugar
 Deposites

 Stool
 Occult blood

96
 METHODOLOGY

 STUDY ENROLEMENT
 In the study, patients reporting at the OPD and IPD of Government Siddha
Medical college and Hospital, Palayamkottai. With the clinical symptoms of
PAANDU will be referred to the research group. Those patients will be screened
using the screening proforma ( Form I) and examined clinically for enrolling in
the study based on the inclusion and exclusion criteria. Based on the inclusion
criteria the patients will be included first and excluded from the study on the same
day if they hit the exclution criteria.
 The patient who are to be enrolled would be informed ( Form IV-A) about the
study, and the objectives of the study in the language and terms understandable
for them.
 After ascertaining the patiet’s willingness, a written informed consent would be
obtaind from them in the consent form (Form IV)
 All these patients will be given unique register card in which patients register
number of the study, Address, Phone number and Doctor phone number etc. will
be givn, so as to report to research group easily if any complication arises.
 Compleete clinical history, complains and duration , examination finding all
would be recorded in the prescribed proforma in the history and clinical
assessment forms separately. Screening Form – I will be filled up , Form I-A,
Form II and Form III will be used recording the patient’s history, clinical
examination of symptoms and signs and lab investigations respectively.

 LAB INVESTIGATION
 Compleete blood test
 Urine test
 Blood Peripheral smears study
 Blood group

 INVESTIGATION DURING THE STUDY

The patient wil be subjected to basic necessary laboratory parameters during the
study.

97
 TREATMENT DURING THE STUDY
Normal treatment procedure followed in Governtment Siddha Medical college
and Hospital, Palayamkottai will be prescripted to the study patient’s and the
treatment will be provide at free of cost.

STUDY PERIOD

 TOTAL PERIOD
 Total period - 24 months
 Recruitment for the study - Upto 18 months
 Data entry analysis - 4 months
 Report preparation and submission - 2 months

DATA MANAGEMENT

 After entrolling the patients in the study, a separate files for each patient will be
open and all forms will be filled in the files. Study No and patient No. Will be
entered top of file for the easy identification and arranged in a separate rack at the
concern OPD unit. whenever study patients visit OPD during the study period,
the respective patients file will be taken and necessary recording will be made at
the assessment form or other suitables form.
 The screening forms will be seperatedely.
 The Data recording will be monitored for completion and adverse event by Head
Of the Department and Faculty of the department. Any missed data found in
during the study, it will be collected form the patient, but the time related data not
be recorded retrospectively.
 All collected data will be analysed using SPSS V 2.0

STATISTICAL ANALYSIS

Data on sign and symptoms, complete blood count ( Hb, WBC, DC, PCV,
MCV, MCH, MCHC) and peripheral smear and other diagnostic stool will be
analysed by using SPSS V 2.0 version.

98
 OUTCOME OF STUDY

According to the references of the text books the diagnostic outcome of the
study includes validation of Siddha diagnostic tools such asNeerkuri, Neikuri,
Envagai thervugal and Manikkadai nool in Paandu with good results.

ETHICAL ISSUES

 To prevent any infection, while collecting blood samples from the patients, only
disposable syringes, disposable gloves , with proper sterilization of lab
equipments will be used.
 The data collected from the patient will be kept confidentially. The patient will be
informed about the diagnosis.
 After the consent of the patients (through written consent form) they will be
entrolled in the study.
 Informed consent will be obtained from the patients explaining in the
understandable language to the patient.
 This study involves only the necessary investigations.
 No other unwanted investigation would be done.
 Normal treatment procedure followed in GSMC and Hospital will be prescribed
to the study patents.
 There will be no infrigement on the rights of patient.

OBSERVATION AND RESULTS

Results were observed with respect of the following aspects.

1. Age distribution
2. sex
3. Religion
4. Diet habbits
5. Educational status
6. Food
7. Udal thathukkal
8. General etiology

99
9. General clinical Sign and symtoms
10. Iymporikal
11. Kanmainthiriyankal
12. Gunam
13. Kosam
14. Uyirththathukkal
I. Vali
II. Azhal
III. Iyam
15. Types of Paandu
16. Noi uttra kaalam
17. Noi utra nilam
18. Envagaithervugal
I. Naa-Suvai, Niram
II. Mozhi
III. Vizhi
IV. Isparism
V. Malam
VI. Mooththiram – Neerkkuri, Neikkuri
VII. Naadi – Kaalam, Naadi nadai
19. Manikkadai nool
20. Blood grouping
21. Phripheral smear

100
OBSERVATIONS AND RESULTS

TABLE – 03. AGE DISTRIBUTION

AGE NO OF
S.NO DISTRIBUTION CASES PERCENTAGE
1 40 – 45 8 20.00%
2 46 – 50 5 12.50%

3 51- 55 7 17.50%

4 56-60 13 32.50%

5 61-65 7 17.50%

14 13

12

10
8
NO OF CASES

8 7 7

6 5

2
20.00% 12.50% 17.50% 32.50% 17.50%
0
40 - 45 46 - 50 51- 55 56-60 61-65
AGE DISTRIBUTION

NO OF CASES PERCENTAGE

101
 TABLE 04 : SEX

SEX NO OF
S.NO DISTRIBUTION CASES PERCENTAGE
1 Male 16 40%

2 Female 24 60%

Sex

25

20

15
NO OF CASES

NO OF CASES
PERCENTAGE
10

0
Male Female
SEX

102
 TABLE 05 : RELIGION

RELIGION NO OF
S.NO DISTRIBUTION CASES PERCENTAGE
1 Hindu 33 82.50%
2 Christian 6 15.00%

3 Muslim 1 2.50%
40

RELIGION

35 NO OF CASES PERCENTAGE

30

25

20

15

10

0
Hindu Christian Muslim

103
TABLE -06 DIET HABBIT

DIET NO OF
S.NO DISTRIBUTION CASES PERCENTAGE
1 Tea 28 70%

2 Coffe 19 47.50%

3 Smoking 6 15%

4 Alcohol 1 2.50%

5 Betelnut 19 47.50%

6 Yoga 1 2.50%

7 Tobbcco 4 10%

DIET HABBIT

30 28

25

20 19 19

15

10

5 4

70% 1 1
47.50% 15% 2.50% 47.50% 2.50% 10%
0
Tea Coffe Smoking Alcohol Betelnut Yoha Tobbcco

NO OF CASES PERCENTAGE

104
 TABLE 07 EDUCATIONAL STATUS
EDUCATION NO OF
S.NO DISTRIBUTION CASES PERCENTAGE
1 Illiterate 9 22.50%

2 Literate 24 60.00%

3 Student 0 0.00%

4 Graduate 7 17.50%

EDUCATION STATUS
7
9
Illiterate
Literate
Student
Graduate

24

TABLE 08 FOOD
FOOD NO OF
S.NO DISTRIBUTION CASES PERCENTAGE
1 Vegetable 7 17.50%

2 Mixed Diet 33 82.50%

FOOD DISTRIBUTION
Vegetable Mixed Diet
33

82.50%
17.50%
7

NO OF CASES PERCENTAGE

105
TABLE 09 UDAL THATHUKKAL
UDAL NO OF
S.NO THATHUKKAL CASES PERCENTAGE
1 Saram 40 100%

2 Senner 40 100%

3 Oon 15 37.5%

4 Kozluppu 15 37.5%

5 Enbu 10 25%
6 Moolai 00 00%

7 Sukkilam/Suronitham 40 00%

UDAL THATHUKKAL

40
35
30
25
20
15
10
5
0

NO OF CASES PERCENTAGE

106
 TABLE 10- GENERAL ETIOLOGY

NO OF
S.NO GENERAL ETIOLOGY CASES PERCENTAGE
1 Poor nutritional Diet 40 100%

2 Alteration on cooking of food 40 100%

3 Alcoholism 1 2.5%

4 Gastro Intestinal Disease 0 0

5 Medication 0 0

6 Malignancy 0 0

40 0

GENERAL ETIOLOGY

Poor nutritional Diet Alteration on cooking of food Alcoholism

107
TABLE 11- GENERAL CLINICAL SYMPTOMS
GENERAL CLINICAL NO OF
S.NO SYMPTOMS CASES PERCENTAGE
1 Stomatities 13 32.5%

2 Pallor of the eyes 36 90.0%

3 Pallor of the lips 17 42.5%

4 Pallor of the face 28 70.0%

5 Pallor of the tongue 11 27.5%

Pallor and dryness of the

6 skin 37 92.5%

7 Anorexia 32 80.0%

8 Palpitation 28 70.0%
9 Lassitute 38 95.0%

10 Tiredness 38 95.0%

11 Bradycardia 0 000%

12 Dyspnoea on exertion 22 55.0%

13 Protusion of eye balls 4 10.0%

14 Ankle oedema 2 5.0%

15 Murmur 0 000%

NO OF CASES PERCENTAG
40

35

30

25

20

15

10

108
 TABLE 12- IYMPORIKAL
NO OF
S.NO IYMPORIKAL CASES PERCENTAGE
1 Mei 30 75%
2 Vaai 22 55%
3 Kan 30 75%
4 Mooku 00 00
5 Sevi 00 00

IYMPORIKAL

30

25

20

15

10

0
Mei Vaai Kan Mooku Sevi

NO OF CASES PERCENTAGE

109
TABLE -13 KANMETHIRIYANGAL
NO OF
S.NO KANMENTHIRIYANKAL CASES PERCENTAGE
1 Kai 20 50%
2 Kaal 20 50%
3 Vaai 22 55%
4 Eruvaai 30 75%
5 Karuvaai 0 0

KANMENTHIRIYANKAL

NO OF CASES PERCENTAGE

30

25

20

15

10

0
Kai Kaal Vaai Eruvaai Karuvaai

110
TABLE 14 - GUNAM
NO OF
S.NO GUNAM CASES PERCENTAGE
1 Saththuvam 0 0

2 Rasatham 08 20%

3 Thamasam 32 80%

GUNAM

35

30

25

20

15

10

0
Saththuvam Rasatham Thamasam

NO OF CASES PERCENTAGE

111
TABLE – 15 KOSAM
NO OF
S.NO KOSAM CASES PERCENTAGE
1 Annamaya Kosam 40 100%
2 Pranamaya Kosam 30 75%

3 Manomaya Kosam 0 00

4 Vinganamaya Kosam 0 00
5 Ananthamaya Kosam 0 00

KOSAM
40

35
NO OF CASES PERCENTAGE

30

25

20

15

10

0
Annamaya Kosam Pranamaya Manomaya Kosam Vinganamaya Ananthamaya
Kosam Kosam Kosam

112
TABLE -16 UYIRTHATHUKKAL
NO OF
S.NO VALI CASES PERCENTAGE
1 Pranan 30 75%

2 Abanan 30 75%

3 Samanan 40 100%

4 Udanan 35 87.50%

5 Viyanan 30 75%

6 Naagan 5 12.50%

7 Koorman 5 12.50%

8 kirukaran 35 87.50%

9 Thevathaththan 35 87.50%

10 Thananjeyan

UYIRTHATHU - VALI
40
NO OF CASES PERCENTAGE

35

30

25

20

15

10

113
TABLE – 17 AZHAL
NO OF
S.NO AZHAL CASES PERCENTAGE
1 Anila piththam 40 100%

2 Ranjaka piththam 40 100%

3 Prasaka piththam 35 87.50%

4 Aalosaka piththam 20 50%

5 Saathaka piththam 0 00

AZHAL

40
NO OF CASES PERCENTAGE

35

30

25

20

15

10

0
Anila Ranjaka Prasaka Aalosaka Saathaka
piththam piththam piththam piththam piththam

114
TABLE – 18 IYAM

S.NO IYAM NO OF CASES PERCENTAGE

1 Avalambagam 30 75%

2 Kilethagam 40 100%

3 Pothagam 15 37.50%

4 Tharppagam 5 12.50%

5 Santhigam 20 50%

UDAL THATHU- IYAM

NO OF CASES PERCENTAGE

40

35

30

25

20

15

10

0
Avalambagam Kilethagam Pothagam Tharppagam Santhigam

115
TABLE – 19 TYPE OF PAANDU
S.NO TYPES OF PAANDU NO OF CASES PERCENTAGE
1 Vathapaandu 5 12.50%

2 Piththapaandu 32 80%

3 Kapapaandu 3 7.50%

4 Vishapaandu 0 0

5 Miruthikapaandu 0 0

TYPE OF PAANDU

35
NO OF CASES

PERCENTAGE
30

25

20

15

10

0
Vathapaandu Piththapaandu Kapapaandu Vishapaandu Miruthikapaandu

116
 TABLE – 20 NOI UTTRA KAALAM
S.NO NOI UTTRA KAALAM NO OF CASES PERCENTAGE
1 Kaarkaalam 1 2.50%

2 Koothirkaalam 5 12.50%

3 Munpanikkaalam 25 62.50%

4 pinpanikkaalam 9 22.50%

5 Illavenirkaalam 0 0

6 Mudthuvenirkaalam 0 0

NOI UTTRA KAALAM

25

20 NO OF CASES PERCENTAGE

15

10

117
TABLE – 21 NOI UTTA NILAM
S.NO NOI UTTRA NILAM NO OF CASES PERCENTAGE
1 Kurinji 3 7.5%

2 Mullai 24 60%

3 Marudham 8 20%
4 Neidhal 5 12.5

5 Paalai 0 0

NOI UTTA NILAM

25

20

15

10

0
Kurinji Mullai Marudham Neidhal Paalai

NO OF CASES PERCENTAGE

118
TABLE – 22 ENVAGAI THERVUGAL
S.NO NAAKKU - SUVAI NO OF CASES PERCENTAGE
1 Inippu 0

2 Uppu 3 7.50%

3 Kaarppu 0

4 Pulippu 5 12.50%

5 Kaippu 32 80%
6 Thuvarppu 0

NAA- SUVAI

NO OF CASES

PERCENTAGE
35

30

25

20

15

10

0
Inippu Uppu Kaarppu Pulippu Kaippu Thuvarppu

119
TABLE – 23 NAA NIRAM
S.NO NIRAM NO OF CASES PERCENTAGE
1 Karuppu 3 7.50%

2 Manjal 4 10%

3 Veluppu 33 82.50%

NIRAM

Karuppu
Manjal
Veluppu

120
TABLE – 24 MOZHI
S.NO MOZHI NO OF CASES PERCENTAGE
1 Sama oli 9 22.50%

2 Uraththa oli 24 60%

3 Thaazhntha oli 7 17.50%

MOZHI
NO OF CASES
PERCENTAGE
30

20

10

0
Sama oli Uraththa oli Thaazhntha oli

TABLE – 25 VIZHI
S.NO VIZHI NO OF CASES PERCENTAGE
1 Manjal 6 15%
2 Veluppu 33 82.50%

3 Sivappu 1 2.50%

Sivappu VIZHI Manjal

2.5% 15%

Manjal
Veluppu
Sivappu

Veluppu
82.5%

121
TABLE – 26 ISPARISAM

NO OF
S.NO ISPARISAM CASES PERCENTAGE
1 Veppam 16 40%

2 Midhaveppam 24 60%

3 Thatpam 0

1 Viyarvai 2 5%

1 Thoduvali 3 7.50%

ISPARISAM

NO OF CASES

25
PERCENTAGE

20

15

10

0
Veppam Midhaveppam Thatpam Viyarvai Thoduvali

122
TABLE – 27 MALAM - THANMAI
S.NO MALAM - THANMAI NO OF CASES PERCENTAGE
1 Karuppu 0 0
2 Manjal 40 100%
3 Velluppu 0 0
1 Ilakal 0 0

2 Irukal 32 80%

3 Thin 6 15%

4 Bulgy 2 5%

MALAM- NIRAM, THANMAI

40

35

30

25

20

15

10

0
Karuppu Manjal Velluppu Ilakal Irukal Thin Bulgy

123
 TABLE – 28 MOOTHTHIRAM - NEIKKURI

MOOTHTHIRAM -
S.NO NEERKKURI NO OF CASES PERCENTAGE
1 Venmai 0 0

2 Sivappu 1 2.50%

3 Manjal 39 97.50%

1 Manam 5 12.5%

2 Nurai 5 12.50%

3 Edai 0 0%

4 Enjal 2 5%

MOOTHTHIRAM - NEERKKURI

40

35

30

25

20

15

10

0
Venmai Sivappu Manjal Manam Nurai Edai Enjal

124
 TABLE – 29 MOOTHTHIRAM - NEIKKURI
MOOTHTHIRAM - NO OF
S.NO NEIRKKURI CASES PERCENTAGE
1 Arvam 3 7.50%

2 Mothiram 4 10%

3 Muththu 2 5%

4 Aravil Mothiram 1 2.50%

5 Aravil muththu 0 0

6 Mothiraththil Aravam 11 27.5%

7 Mothiraththil Muhthu 17 42.50%

8 Muththil Aravam 2 5%

9 Muththil mothiram 0

18

16

14

12

10

125
TABLE – 30 NAADI - KAALAM
NAADI - NO OF
S.NO KAALAM CASES PERCENTAGE
1 Kaarkaalam 2 5%

2 Koothirkaalam 2 5%
3 Munpanikkaalam 18 45%

4 Pinpanikkaalam 13 32.50%

5 Ilavenitkaalam 4 10%

6 Mudhuvenitkaalam 1 2.50%

NAADI - KAALAM

Kaarkaalam Koothirkaalam Munpanikkaalam

Pinpanikkaalam Ilavenitkaalam Mudhuvenitkaalam

126
TABLE – 31 NAADI – NAADI NADAI
NAADI - NADI NO OF
S.NO NADAI CASES PERCENTAGE
1 Vali 0 00%

2 Azhal 0 00%

3 Iyam 0 00%
4 Valiazhal 12 30%

5 Valiaiyam 0 00%

6 Azhalvali 23 57.50%

7 Azhalaiyam 4 10%

8 Iyavali 1 2.50%

9 Iyaazhal 0 00%

10 Sanni 0 00%

NAADI - NADI NADAI

25

20

15

NO OF CASES
10 PERCENTAGE

127
TABLE – 32 MANIKKADI NOOL

S.NO SIZE MALE FEMALE

1 71/4 2 8

2 7 1/2 0 1

3 8 0 1

4 8 1/4 0 1

5 8 1/2 2 4
6 8 3/4 3 2

7 9 1 2

8 9 1/4 3 2
9 9 1/2 4 2

10 9 3/4 1 1

Chart Title
10

0
1 2 3 4 5 6 7 8 9 10

SIZE MALE FEMALE

128
TABLE – 33 TABLE BLOOD GROUPING

Rh Rh
A/ A Positi negati
A1 B O B ve ve
VATHA
PAANDU 2 2 0 1 5

PITHTHA 1
PAANDU 4 6 7 5 31 1

KAPA
PAANDU 1 0 2 0 3

35

30

25

A/A1
20 B
O
AB
15 Rh Positive
Rh negative

10

0
VATHA PAANDU PITHTHA PAANDU KAPA PAANDU

129
TABLE – 34 PERIPHERAL SMEAR

Piththam
Vatham

P Percentage
ePercentage

Percentage
TOTAL Total

Kapam
ANAEMIA
TYPES ( case) P PERCENTAGE

IRON
DEFICIENCY 2 5% 14 35% 1 2.50% 17 42.50%

HYPOCHROMIC
MICROCYTIC 3 7.50% 15 37.50% 1 2.50% 19 47.50%

OTHERS 0 3 7.50% 1 2.50% 04 10%

PERIPHERAL SMEAR
16

14

12
Vatham

10 Percentage
Piththam

8 Percentage
Kapam
6 Percentage
TOTAL
4 Total PERCENTAGE

0
IRON DEFICIENCY HYPOCHROMIC OTHERS
MICROCYTIC

130
131
132
133
134
135
136
 TABLE – 35 ENVAGAI THERVUGAL AND MANIKKADAI NOOL

ISPARISAM
MOZHI
NIRAM

VIZHI
AG SE NEERKUR MANIKKAD
S.NO

OP.NO NAA MALAM NEIKURI NAADI

E X I AI

1 32819 65 F O/KI/VD MN UO MN VP MN/IR MN MOMU IK/VP/ML/VI/AV LF 8 1/2

2 34932 58 F MN/KI VL UO VL VP MN/IR MN/NU MO IK/VP/ML/VI/AV LF 9 1/4

3 35206 40 F MP/VL/UP VL SO VL MD MN/BL MN MU IK/VP/IY/MI/VA LF10

MP/VL/UP/V
4 35402 48 F D VL TO VL MD MN/BL MN MUA IK/VP/ML/VI/VA LF 9

MP/VP/ML/VI/A
5 9319 60 M MN/KI VL SO VL VP MN/IR MN MOMU V RT 8 3 /4

6 9321 65 M VL/KI/VD VL SO VL MD MN/IR MN MOA MP/VP/IY/VI/AV RT 9

7 9750 60 F VL/KI VL UO VL MD MN/IR MN/NU MOMU MP/VP/IY/VI/AV LT 8 1/2

8 9751 65 F MN/KI VL UO VL MD MN/IR MN MOMU MP/VP/IY/VI/AV LF 7 1/4

MN/IR/D PP/VP/ML/VI/A
9 11134 40 F MN/KI/VD VL UO MN MD E MN MO V LF 9 1/2

10 11439 50 F VL/KI MN UO MN MD MN/IR MN MOA MP/VP/IY/VI/AV LF 8

11 11440 59 M MN/KI VL UO VL VP MN/IR MN MOMU MP/VP/IY/VI/VA RT 9 1/4

12 11442 40 F VL/KI VL UO VL MP MN/IR MN MOMU MP/VP/IY/VI/AI LF 8 3/4

137
 ISPARISAM
MOZHI
NIRAM

VIZHI
AG SE NEERKUR MANIKKAD
S.NO
OP.NO NAA MALAM NEIKURI NAADI
E X I AI

MP/VP/ML/VI/A
13 11615 60 F MN/KI VL UO VL VP MN/IR MN MOMU V LF 7 1/4
14 11616 63 M VP/MN VL SO VL VP MN/IR MN MOA MP/VP/IY/VI/VA RT 9 1/4

MP/VP/ML/VI/A
15 11617 52 F MN/KI VL UO MN VP MN/IR MN MOMU V LF 8 3/4
16 11618 61 M MN/KI VL SO VL MP MN/IR MN MOA MP/VP/IY/VI/AV RT 9 12

17 13510 40 M KA/PU/VD KA UO SP VP MN/TN MN/NU MOA PP/VP/IY/VI/VA RT 9 3/4

MP/VL/KI/V PP/VP/ML/VI/A
18 13511 60 M D VL UO VL MP/TV MN/IR MN MUA V RT 9 1/2

PP/VP/ML/MI/A
19 14850 58 F MN/KI VL SO VL MP MN/IR MN MO V LF 7 1/4
20 14851 52 F MN/KI VL TO VL MP MN/IR MN MOA PP/VP/IY/MI/VA LF 8 3/4

21 14852 51 F MN/KI VL UO VL VP MN/IR MN MO PP/VP/IY/VI/AI LF 9

22 15165 65 M MN/KI VL UO VL MD MN/TN MN A PP/VP/IY/VI/VA RT 9 1/4

23 15166 50 F MN/KI VL UO VL MD MN/IR MN MOA PP/VP/IY/VI/VA LT 7 I/4

PP/VP/VV/MN/A
24 16114 45 F MN/KI/VD MN TO MN VP MN/IR MN MOMU V LT 9

138
 ISPARISAM
MOZHI
NIRAM

VIZHI
AG SE NEERKUR MANIKKAD
S.NO
OP.NO NAA MALAM NEIKURI NAADI
E X I AI

PP/VP/ML/MN/A
25 16115 60 F VL/KI/VD MN UO MN VP MN/IR MN MOMU V LT 9 1/4
PP/VP/ML/VI/A
26 16586 60 M MP/VL/KI VL SO VL MD MN/IR MN MOMU V RT 7 1/4

PP/VP/ML/VI/V
27 16589 60 M VL/KI VL UO VL VP MN/IR MN MOA A RT 8 3 /4

28 16590 62 M MN/KI VL UO VL MD MN/IR MN MOMU PP/VP/IY/VI/AV RT 8 1/2

MD/T
29 16592 45 M VL/PU/VNU KA UO VL V MN/TN MN MOA PP/VP/IY/VI/VA RT 9 1/4

30 16635 46 M VL/KI VL TO VL VP/VY MN/IR MN MOMU PP/VP/IY/MI/AI RT 9 1/2

MD/V PP/VP/VV/MN/A
31 18601 40 F MN/UP/VD VL TO VL Y MN/BL MN MU V LT 9 1/2

PP/VP/IY/MN/V
32 18967 58 M KA/PU/VD KA SO VL MD MN/TN MN AMO A RT 8 1/2
MOMU PP/VP/VV/MN/A
33 21052 55 F MN/KI/VD VL TO VL VP/TV VL/IR MN/EN PP/VP V LT 7 1/4

34 21151 55 F VL/KI VL TO VL VP MN/IR MN MOMU PP/VP/ML/VI/AI LT 8 1/2

MP/VL/KI/V
35 21178 48 F D VL UO VL MD MN/TN MN MOA PP/VP/IY/VI/IV LT 8 1/2

139
 ISPARISAM
MOZHI
NIRAM

VIZHI
AG SE NEERKUR MANIKKAD
S.NO
OP.NO NAA MALAM NEIKURI NAADI
E X I AI

PP/VP/ML/VI/V
36 21290 52 M MN/KI VL UO VL MD MN/IR MN MOA A RT 9 1/2
37 21291 58 F VP/KI VL SO VL MD MN/IR MN MOMU PP/VP/IY/VI/AV LF 7 1/2

38 21294 59 M KA/PU/VNU VL UO VL MD MN/TN MN/NU A PP/VP/IY/VI/VA RT 7 1/4

39 21295 55 F MN/KI VL UO VL MD MN/IR MN MOA PP/VP/IY/VI/AV LT 8 3/4

PP/VP/ML/VI/A
40 32057 40 F VP/KI VL UO VL MD MN/IR MN/NU MOMU V LT 8 1/4

M – Male F – FEMALE KP- KARUPPU MN- MANJAL VL – VELUPPU O- OTHERS IR- IRUKAL

TN – THIN BL – BULKY IN – INIPPU UP – UPPU KI – KAIPPU PU – PULIPPU

TU – TUVARPPU VNU – VAAI NEER URAL VD – VEDDIPPU VN – VENMAI NU – NURAI

EN – ENJAL SI – SIVAPPU MN – MANAM ED- EDAI K - KANNEE

E – ERACHCHAL PS - PEELAI SAARUTHAL MD – MIDHAVEPPAM VP – VEPPAM

TP- THATPAM TV – THODUVALI VY – VIYARVAI DE – DECREASED VA – VALIAZ –
AZHAL IY – IYAM VA- VALIAZHAL VI – VALIIYAM AV – AZHAL VALI

140
AI – AZHALIYAM IV – IYAVALI IA – IYAAZHAL SA – SAMAOLI UO – URATHTHA OLI

TO – THAZHLNTHA OLI KA – KAARKAALAM KO – KOOTHIRKAALAM MP – MUNPANIKKAALAM

PP – PINPANIKKAALAM IV – ILAVENITKAALAM MV – MUTHUVENITKAALAM KU – KULIR VP – VEPPAM

IY – IYALPU VV- VALIVU ML – MELIVU A – ARAVAM

MO- MOTHIRAM MU- MUTHTHU AMO- ARAVIL MOTHIEAM AMU – ARAVIL MUTHTHU

MOA- MOTHIRATHTHIL ARAVAM MOMU – MOTHIRATHTHIL ARAVAM MUA – MUTHTHIL ARAVAM

MUMO – MUTHTHIL MOTHIRAM

141
 TABLE – 36
BLOOD URINE

P. SMEAR
RBC HB PCV MCV MCH MCHC TC N L E ESR SUGAR UREA S.CHOLES ALBUM SUGA DEPO
S.NO

OPD

GROUP
m/mm3 g/dl % fl pg gdl cls/mm3 % % % mm/hr mg/dl mg/dl mg/dl ce

1 32819 3.59 9.9 25.8 87.5 27.6 31.5 5900 83 13 1 40 NMA B 104 R 30 198 NIL NIL NAD

2 34932 2.8 8.6 25.8 87.7 26.5 34.2 7700 74 20 4 26 HMA A 90 F 12 196 TRACE NIL 10 pu

3 35206 2.9 8.9 26.7 82.4 26.5 32.9 6900 66 30 3 16 HMA O 120 R 10 198 NIL NIL NAD

FUL
4 35402 2.95 91 27.2 80.9 24.3 32.3 7900 59 9 2 64 IDA O 76 R 30 186 TRACE NIL
PUS

5 9319 3 9.2 27.8 87.5 26.3 33 5900 50 49 1 4 HMA A 99 F 18 135 NIL NIL NAD

6 9321 2.95 9 26.8 83.5 27.6 33.8 8100 69 27 4 20 HMA B 76 F 65 183 FEW NIL 18 P

7 9750 2.66 8 24 78.4 23.2 33.7 6000 57 7 6 135 SIDA B 128 R 60 162 NIL NIL FEW

8 9751 3.3 10 29.8 74.5 25.4 33.2 6500 68 28 4 81 IDA B 522 R 25 180 FEW B.RED 15 P

9 11134 2.2 6.6 19.8 70.1 22.4 31.7 8100 63 33 4 20 HMA A 96 F 28 190 NIL NIL NAD

10 11439 2.7 8 24.8 83.5 27.4 33.5 8400 73 23 4 10 HMA B 93 F 30 160 NIL NIL NAD

11 11440 3.32 10 30.4 90.3 28.4 34.7 8800 70 20 10 68 DMPA O 114 R 18 162 TRACE NIL 10PU

12 11442 2.9 8.7 26.1 88.2 28.1 33.9 6900 67 28 5 33 HMA AB 84F 26 158 NIL NIL FEW

13 11615 2.96 8.9 26.7 85.8 27.6 33.2 10500 85 13 2 15 IDA AB 85 F 20 140 NIL NIL NAD

142
 BLOOD URINE

RBC HB PCV MCV MCH MCHC TC N L E ESR

P. SMEAR
SUGAR UREA S.CHOLES ALBUM SUGA DEPO
S.NO

OPD

GROUP
m/mm3 g/dl % fl pg gdl cls/mm3 % % % mm/hr mg/dl mg/dl mg/dl ce

14 11616 3.31 10 30.2 87.5 28.6 33.8 6100 65 31 4 16 HMA O 187 R 18 220 NIL NIL NAD

15 11617 3.53 10 31.8 82.3 27.5 32.4 6100 67 30 3 92 HMA A 7O R 30 224 TRACE NIL CAL

16 11618 3.2 9.6 28.8 89.5 28.1 33.6 7500 63 34 3 20 DMPA B 102 R 25 152 NIL NIL NAD

17 13510 3.2 9.8 29.4 82.4 25.5 32.1 7500 60 36 4 30 HMA B 68 R 28 168 NIL NIL NAD

18 13511 3.1 9.3 27.9 83.2 28.1 34.5 8400 65 33 2 10 IDA B 92 R 32 182 NIL NIL NAD

19 14850 2.86 8.6 25.8 82.3 25.4 32.8 9400 69 25 5 50 IDA B 147R 18 196 NIL NIL 3 PU

20 14851 3.35 10 30.3 86.4 28.1 34.2 6300 58 40 2 50 HMA B 270 F 58 240 NIL B.RED NAD

21 14852 3.35 8 30.3 76.4 22.7 34.6 7300 70 24 6 19 SIDA B 73 R 22 196 NIL NIL NAD

22 15165 2.5 7.6 22.8 89.4 27.6 33.3 9500 79 18 3 128 HMA AB 74 F 78 145 TRACE NIL 5 PU

23 15166 2.95 9 26.8 85.4 25.9 32.1 8700 75 22 3 55 HMA 0 121 R 32 128 NIL NIL 2 PU

24 16114 3.2 9.9 29.7 79.4 26.2 33.3 5900 53 43 4 32 IDA AB 83 F 20 215 NIL NIL NAD

25 16115 3.3 10 29.7 72.3 21.4 30.5 5100 70 27 3 70 SIDA O 140 R 32 204 NIL NIL NAD

26 16586 3.3 9.9 29.7 80.1 24.3 34.5 6600 68 30 2 20 SIDA B 79 F 22 171 NIL NIL FEW

27 16589 2.8 8.4 25.2 73.5 24.7 34.1 10500 70 20 10 90 IDA O 111 R 18 203 NIL P 5 PU

28 16590 3.1 9.3 27.9 89.3 26.6 34.1 5300 53 40 7 60 HMA B 144 R 30 140 TRACE NIL FEW

29 16592 3.33 10 30.1 78.9 22.3 33.9 8800 67 27 6 125 IDA A 75 R 18 162 POSITV NIL FEW

143
 BLOOD URINE

RBC HB PCV MCV MCH MCHC TC N L E ESR

P. SMEAR
SUGAR UREA S.CHOLES ALBUM SUGA DEPO
S.NO

OPD

GROUP
m/mm3 g/dl % fl pg gdl cls/mm3 % % % mm/hr mg/dl mg/dl mg/dl ce

30 16635 2.83 8.4 25.2 78.6 23.5 30.9 8100 73 20 7 70 IDA B 111 R 34 207 NIL NIL NAD

31 18601 2.83 8.5 25.2 89.2 27.8 33.4 6500 61 28 2 20 DMPA A1 105 R 12.5 175 NIL NIL NAD

32 18967 3.26 9.8 29.4 87.5 26.3 33 9900 69 30 1 60 HMA A 87 R 37 179 NIL NIL FEW

33 21052 2.95 9 26.5 82.3 24.8 33.7 6600 57 40 3 45 IDA O 160 F 22 223 NIL NIL 3 PU

34 21151 2.7 9.4 24.8 83.5 27.4 33.5 9000 69 22 9 40 HMA B 140 R 23 171 NIL NIL NAD

35 21178 2.8 8.6 25.8 88.5 29.4 34.5 8300 70 23 7 110 HMA AB 80 F 48 182 NIL NIL NAD

36 21290 3.36 10 30.4 87.2 28.7 32.8 9200 60 31 9 30 HMA AB 70 R 48 170 NIL NIL NAD

37 21291 3.23 9.7 29.1 80 23.5 31.2 6600 60 37 3 28 IDB12F O 117 R 28 241 NIL NIL FEW

38 21294 3.26 9.8 29.4 83.2 26.5 33.3 7400 67 30 3 140 IDA B 314 R 28 152 NIL B.RED FEW

39 21295 3.16 9.5 28.5 77.4 23.5 32.9 10400 50 32 18 80 SIDA B 200 R 38 240 TRACE YELLOW 10 P

40 32057 3.26 8.2 29.4 83.2 26.5 33.3 7800 68 29 2 90 IDA B 138 R 20 224 NIL NIL NAD

144
DISCUSSION
40 Cases of Paandu noi have taken for clinical study in the Noinadal Post-
graduate Out Patient Department of Government Siddha Medical College and
Hospital, Palayamkottai. In this study by author analysed the clinical features,
depicted in the poem “Agasthiyar gunavaakadam” about PAANDU NOI.

1. Sign and symptoms

TABLE – 37

Vaathappaandu No . cases Piththapaandu No.cases Kapapaandu No cases

pain in the 05 Yellowish 32 Shining of the 03

extremities and colouration of the skin
abdomen body, eyes, nail
and urine
Oedema of 01 Mood swing loss 01 Oedema of 03
eyes, face and of intelligence feet and
arm dorsum of the
hand
Pallor of the Pallor of the stool Absent Pallor of the 03
body 05 eye, face,

Lassitude 05 Lassitude 30 Lassitude 03

Dyspnoea 05 Dyspnoea 17 Swelling of Absent
tongue
Vomiting 05 Memory loss 20 Abdomeinal 01
swelling
Hic cough 05 Tiredness 32 Huskey voice 03
Excessive 05 Giddiness 08 Giddiness 02
salivation
Body itching 30 Pallor of the Absent
urine and
faecies

145
 Bitter in taste 32 Excessive 02
sweating
Emaciation 26 Chillness of Absent
eyes
Thoracic pain 01
Anasarca Absent
Chest pain Absent

 Out of 40 cases, pain in the extremities and abdomen , Oedema of eyes, face and
arm , Pallor of the body ,Vomiting, Hic cough and Excessive salivation are present
special sign and symptoms of the Vathappaandu. These symptoms are not present
in other types of Paandu. By author consider this type of paandu noi is
Vaathapaandu.

 Out of 40 cases, Yellowish colouration of the body, eyes, nail and urine, Mood
swing, loss of intelligence, Memory loss, Tiredness, Body itching, Bitter in taste
and Emaciation are present special sign and symptoms of the Piththapaandu.
These symptoms are not present in other types of Paandu. By author consider this
type of paandu noi is Piththapaandu.

 Out of 40 cases, Shining of the skin, Oedema of feet and dorsum of the hand,
Abdominal swelling, Huskey voice, Excessive sweating and Thoracic pain are
present special sign and symptoms of the Kaphapaandu. These symptoms are not
present in other types of Paandu. By author consider this type of paandu noi is
Kaphapaandu.

2. Envagai thervukal

2.1 NAA :- Out of 40 cases

2.1.1 Naa- niram

 Veluppu is present in 80% cases– By author considering veluppu colour tongue

is indicate the Kapapaandu.
146
 Manjal is present in 10% cases - By author considering Manjal colour tongue is
indicate the Pithapaandu.
 Karuppu is present in 10% cases - By author considering Karuppu colour tongue
is indicate the Vathapaandu.

2.1.2 Naa - suvai

 Kaippu is present in 80% of cases - By author considering Kaippu suvai is indicate

the Piththapaandu
 Pulippu is present in 12.5% of cases - By author considering Pulippu suvai is
indicate the Vathapaandu
 Uppu is present in 7.5% of cases - By author considering Kaippu suvai is indicate
the Kapaandu

2.2 NIRAM: Out of 40 cases:

 Veluppu is present in 82.5% cases - By author considering veluppu colour is

indicate the Kapapaandu
 Manjal is present in 10% cases - By author considering Manjal colour is indicate
the Pithapaandu
 Karuppu is present in 7.5% cases - By author considering Karuppu colour is
indicate the Vathapaandu

2.3 MOZHI : Out of 40 cases;

 Uraththa ozhli is present in 60% of cases - By author considering Uraththa ozhi

is indicate the Pithapaandu
 Samaozhli is present in 22.5% cases - By author considering Sama ozhi is indicate
the Vathapaandu
 Thaazhlntha oli is present in 17..5% cases - By author considering Thazhlntha oli
is indicate the Kapapaandu

2.4 VIZHI : Out of 40 cases;

 Veluppu is present in 82.5% cases - By author considering veluppu colour is

indicate the Kapapaandu
147
 Manjal is present in 15% cases - By author considering Manjal colour is indicate
the Pithapaandu
 Sivappu is present in 2.5% cases - By author considering Sivappu colour is
indicate the Vathapaandu

2.5 ISPARISAM : Out of 40 cases;

 MidhaVeppam is present in 60% cases - By author considering Midhaveppam is

indicate the Piththapaandu
 Veppam is present in 40% cases - By author considering Veppam is indicate the
Vaathapaandu

2.6 MALAM : Out of 40 cases;

2.6.1 malam - Niram

 Manjal colour malam is present in 100% of cases By author considering Manjal

colour malam is indicate the Pithapaandu
 Karuppu and veluppu malam is absent in this cases

2.6.2 Malam – Thanmai

 Irukal is present in 80% cases - By author considering Irukal malam is indicate

the Piththapaandu
 Thin is present in 15% of cases – By author considering Thin malam is indicate
the Vathapaandu
 Bulgy is present in 5% of cases By author considering Bulky malam is indicate
the Kapapaandu

2.7 MOOTHTHIRAM : Out of 40 cases;

2.7.1 Neerkuri

 Manjal is present in 97.5% of cases - By author considering Manjal colour

Mooththiram is indicate the Piththapaandu
 Sivappu is present in 2.5% of cases - By author considering Sivappu colour
moththiram is indicate the Piththapaandu
148
 2.7.2 Neikkuri

 Mothiraththil muththu is present in 42.5% of cases – It is indicate the Piththa

kapham. but 1st seen in Mothiram :- By author considering Piththapaandu
 Mothiraththil aravam is present in 27.5% cases – It is indicate the Piththavatham.
but 1st seen in Mothiram :- By author considering Piththapaandu.
 Mothiram is present in 10% of cases - By Author considering it indicate the
Piththapaandu
 Aravam is present in 7.5% cases – By Author considering It is indicate the Vaatha
paandu.
 Muththil Aravam is present in 5% cases – It is indicate the kapha vaatham. but
1st seen in Muththu :- By Author considering Kaphaapaandu
 Muththu is present in 5% of cases – By Author considering Kaphapaandu
 Aravil Mothiram is present in 2.5% cases– It is indicate the Vathapiththm. but 1st
seen in Aravam :- By author considering Vathapaandu

2.8 NAADI : Out of 40 cases;

 Azhalvali is present in 57.5% of cases

 Valiazhal is present in 30% of cases

 Azhalaiyam is present in 10% of cases
 Iyavali is present in 2.5% of cases

3. UDAL THATHUKKAL : Out of 40 cases;

 Saaram is affected in 100% of cases

 Senneer is affected in 100% of cases
 Oon is affected in 37.5% of cases
 Kozluppu is affected in 37.5% of cases
 Enbu is affected in 25% of cases

– Saaram and Senner are affected in 100 % of cases. By Author considering this
result is indicate the Paandu noi.

149
 4. UYIRTHTHATHUKKAL : Out of 40 cases

4.1 Vali

 Samanan is affect the 100% of cases

 Udanan, Kirukaran and Thevthaththan are affect in 87.5% of cases
 Piranan, Abanan and Viyanan are affect in 75% of cases
 Naagan and Koorman are affect in12.5 % of cases
Decreased Samanan cause vomiting, lassitude, excessive salivation.
Decreased Uthanan cause Dyspnoea, Hic cough
Decreased Kirukaran causes sneezing, dryness of mouth
Decreased Thevathaththan causes lassitude ,
Decreased Pranan causes dyspnea, cough
Decreased Abanan causes constipation
Decreased Viyanan causes pallor of the body

Derangement of Vali causes vomiting, lassitude, excessive salivation,

Dyspnoea, Hic cough, sneezing, dryness of mouth, lassitude, dyspnea, cough,
constipation, pallor of the body. Author considering this result is indicate in
Paandu noi

4.2 Azhal

 Ranjaka piththam is affected in 100% of cases

 Prasaka piththam is affected in 87.5% of cases
 Aalosaka piththam is affected in 50% of cases
 Anila piththam is affected in 40% of cases

Decreased Anal piththam causes loss of appitite

Decreased Ranjaka piththam causes pallorness

Decresed Pirasaka piththam causes skin dryness, itching

Decreased Alosaka piththam causes vision problem, pallor of the eye

Derangement Azhal causes loss of appitite, pallarness, skin dryness,

itching, vision problem, pallor of the eye. Author considering this result is indicate
in Paandu noi

150
 4.3 Iyam

 Kilethagam is affected in 100% of cases

 Avalambagam is affected in 75% of cases
 Pothagam is affected in 37.5% of cases
 Tharppagam is affected in 12.5% of cases
Decreased Kilethagam causes loss of appitite
Decreased Avlambagam causes dyspnea, cough
Decreased Santhigam causes upper and lower limb pain
Decreased Pothagam causes suppression of taste
Decreased Thatpagam is affected Giddiness, eye problems

Derangement of Iyam causes loss of appitite, dyspnea, cough, upper and

lower limb pain, suppression of taste, Giddiness, eye problems. By author
considering this result is indicate in Paandu noi.

5. MUKKUTTA VERUPAADU

 Finally By author discusses,

 Out of 40 cases, Piththapaandu is present in 80% of cases
 Out of 40 cases,Vathapaandu is present in 12.5% of cases
 Out of 40 cases, Kapap paandu present in 7.5% of cases

6. MANIKKADAI NOOL
 71/4 Viratkadai is present in 25% of cases
 71/2 Viratkadai is present in 2.5% of cases
 8 Viratkadai is present in 2.5% of cases
 81/4 Viratkadai is present in 2.5% of cases
 81/2 Viratkadai is present in 15% of cases
 83/4 Viratkadai is present in 12.5% of cases
 9 Viratkadai is present in 7.5% of cases
 91/4 Viratkadai is present in 12.5% of cases
 91/2 Viratkadai is present in 15% of cases
151
 93/4 Viratkadai is present in 5% of cases

According to the Siddha text is described 71/4 Viratkadai indicate the Hip
pain, Pain, Stiffness, eye ache, PAANDU, SOKAI, Burning sensation of the hand
and leg , Excessive sleep. By Author considering 25% of cases have 7 1/4
viratkadai in the Paandu noi.

7. PERIPHERAL SMEAR – Out of 40 cases

 32 piththa cases (80%) is contain 35% iron deficiency anaemia, 37.5%

Hypochromic microcytic Anaemia and 7.5% of iron and B12 deficiency anaemia
is present
 5 vaatha cases (12.5%) is contain 5% iron deficiency anaemia, and 7.5%
Hypochromic microcytic Anaemia is present.
 3 Kapha cases ( 7.5%) is contain 2.5% iron deficiency anaemia, 2.5%
Hypochromic microcytic Anaemia and 2.5% of iron and B12 deficiency anaemia
is present.

Out of 40 cases, mostly affected 47.5% of cases in Hypochromic

microcytic Anaemia and 42.5% of cases in Iron deficiency of anaemia. By author
considering most of the paandu noi present in Hypochromic and Microcytic
anaemia. Specifically 37.5% of patients are affected in piththapaandu.

By author considering paandu noi present in Iron deficiency anaemia.

Specifically 35% of patients are affected in piththapaandu

8. BLOOD GROUPING –

 Out of 40 cases
 32 piththa (80%) cases is contain 40% of cases in B blood group, 17.5% of cases
in O blood group, 12.5% of cases in AB blood group and 10% of cases A/A1
blood group.
 5 Vatha cases (12.5%) is contain 5% of cases in B blood group, 5% of cases in
A blood group and 2.5% of cases in AB blood group
 3 Kapa cases (7.5%) is contain 5% of cases in O blood group and 2.5% of cases
in A1 blood group.
152
 Out of 40 cases
 97.5% of cases Rh positive
 2.5% of case Rh negative

Out of 40 cases, mostly affected 45% of cases in B positive blood group. By

author considering most of the paandu noi present in B positive. Specifically 40%
of patients are affected in piththapaandu.

153
 SUMMARY
Various aspects of examination including Mukkuttam, Udal Thathukkal,
Envagai thervugal are done recorded as proof.

 Interpretation of Etiology – Out of 40 cases

 100% of cases in Poor nutritional Diet and Alteration on cooking food
 2.5% of case in Alcoholism

Maximum number of cases are recorded with Poor nutritional Diet and
Alteration on cooking food habits which may be major causative factor for the
disease of Paandu
 Interpretation of Sign and Symptoms

100% cases depicted the major signs and symptoms as mention in the
poem “PAANDU” in the text book “Agasthiyar Gunavaakadam” Among 40
cases

 95% of cases in lassitude and tirednes,

 92.5% cases in pallor and dryness of the skin,
 90 % of cases in Pallor of the eyes,
 80% of cases in Anoroxia,
 70% of cases in pallor of the face and Palpitation
 55% of cases in dyspnea on exertion.
 42.5% of cases in Pallor of the lips
 32.5% of cases in Stomatities
 27.5% of cases in Pallor of the Tongue
 10% of cases in Protusion of eye ball
 5% of cases in Ankle oedema

 Interpretation of Age
 Paandu prominently found to occur in the age between 56- 60 years are affected
in 32.5% of cases
 40 to 45 years of age are affected in 20% of cases
 51 to 55 years and 61 to 65 years of age are affected in 17.5% of cases

154
 46 to 50 years of age are affected in 12.5% of cases .

 Interpretation of Sex
 Out of 40 cases Paandu prominently found to occur in 60% of female cases are
affected.
 Out of 40 cases 40% of male cases are affected.

 Interpretation of Religion
 Out of 40 cases Paandu noi mostly affected 82.5% of cases in Hindu religion
 Out of 40 cases Paandu noi affected 15% of cases in Christian religion
 Out of 40 cases Paandu noi affected 2.5% of cases in Muslim religion

 Interpretation of Educational status

 Out of 40 cases, Paandu noi is mostly present in 60% of cases in literate
 Out of 40 cases, Paandu noi is present in 22.5% of cases in Illiterate
 Out of 40 cases, Paandu noi is mostly present in 17.5% of cases in Graduate.

 Interpretation of food habit

 Out of 40 cases , Paandu noi is prominently found occur in 82.5% of cases in
mixed diet
 Out of 40 cases , Paandu noi is prominently found occur in 17.5% of cases in
vegetable diet

 Interpretation of Personal habits

 Out of 40 cases, prominently found to occur in 70% of cases use in Tea
 Out of 40 cases, found to occur in 47.5% of cases use in coffee and betelnut
 Out of 40 cases, found to occur in 15% of cases use in smoking
 Out of 40 cases, found to occur in 10% of cases use in Tobacco
 Out of 40 cases, found to occur in 2.5% of cases use in Alcohol
 Out of 40 cases, found to occur in 2.5% of cases habbit in Yoga

 Interpretation of Iymporikal
 Out of 40 cases, mostly affected 75% of cases in mei and kan

155
 Out of 40 cases, affected 55% of cases in Vaai
 Interpretation of Kanmainthiriyankal
 Out of 40 cases, mostly affected 75% of cases in eruvaai
 Out of 40 cases, affected 55% of cases in vaai
 Out of 40 cases, affected 55% of cases in kai and kaal

 Interpretation of Gunam
 Out of 40 cases, mostly prominent in 80% of cases in Thamasam
 Out of 40 cases, prominent in 20% of cases in Rasatham.

 Interpretation of Kosam
 Out of 40 cases, prominently found in 100% of cases in Annamaya Kosam
 Out of 40 cases, found in 75% of cases in Piranamaya kosam

 Interpretation of Uyirthathukkal –
 Out of 40 cases in vali ,
 Samanan is affected in 100% of cases
 Uthanan is affected in 87.5% of cases
 Kirukaran is affected in 87.5% of cases
 Thevathaththan is affected in 87.5% of cases
 Pranan, Abanan and Viyanan are affected in 75% of cases
 Nagan and Koorman are affected in 12.5% of cases

 Out of 40 cases in AZHAL

 Anal piththam and Ranjaka piththam are affected in 100% of cases
 Prasaka piththam is affected in 87.5% of cases
 Alosaka piththam is affected in 50% of cases

 Out of 40 cases in IYAM

 Kilethagam is affected in 100% of cases
 Avalambagam is affected in 75% of cases
 Santhigam is affected in 50% of cases
 Pothagam is affected in 37.5% of cases

156
 Thatpagam is affected in 12.5% of cases

 Interpretation of Udal thathkkal

 Saram is affected in 100% of cases
 Senner is affected in 100% of cases
 Oon is affected in 37.5% of cases
 Kozhuppu is affected in 37.5% of cases
 Enbu is affected in 25% of cases
 Moolai , Sukkilam and Suronitham are not affected in this cases

Derangement of udal thathukkal causes Pallorness of the skin, eye, Weight

gait, Drowsiness, headache, loss of appitite, hair fall, lower and upper limb pain
and all joints pain.

 Interpretation of Noi utta Kalam (seasonal variation) - Out of the 40% Paandu
 Paandu prominently found to occur in 62.5% of cases are affect in
Munpanikkalam
 22.5% of cases are affected in pinpanikkalam
 12.5% of cases are affected in Koothikalam
 2.5% of cases are affected in Kaarkaalam

 Interpretation of Noi utta nilam

 Out of 40 cases, Panndu is prominently afeected 60% of cases in Mullai nilam
 Out of 40 cases, Panndu is afeected 20% of cases in Marudha nilam
 Out of 40 cases, Panndu is afeected 12.5% of cases in Neithlal nilam
 Out of 40 cases, Panndu is prominently afeected 7.5% of cases in Kurinchi nilam

 Interpretation of ENVAGAI THERVUGAL

 Naa – Tongue is plays a major roles in the diagnosis of Paandu
 Velluppu of the tongue is present in 82.5% of cases
 Fissure (Vedippu) is present in 30% of cases
 Kaippu present in 80% of cases
 Vaai neer ooral 5% of cases.

Fissures dryness, black pigmentation due to Vatha constitution

157
 Pallorness due to impaired Ranjaka Piththam
Suppression of taste due to Kabha constitution

 Interpritation of NIRAM
 Pallorness (velluppu) of the skin noted in 82.5% of cases
 Yelow colouration of the skin noted 10% of cases
 Black colouration of the skin is noted 7.5% of cases

Skin also one of the main indicator of Paandu.

Pallorness of the skin due to impaired Ranjaka piththam.

 Interpretation of Mozhi
 60% of cases are with Uraththa oli
 22.5% of cases are with Sama oli
 17.5% of cases are with Thaazhntha oli

Speech affected in Paandu due to derangement in mukkuttam

 Interpretation of Vizhi
 Pallorness of conjunctiva noted in 82.5 % of cases
 Yellow colouration of conjunctiva noted in 15 % of cases
 Red colouration of conjunctiva noted in 2.5 % of cases

Pallorness of conjunctiva due to Ranjaka Piththam decreased state.

 Interpretation of Isparism
 60% of cases are Midha veppam in nature
 40% of cases are veppam in nature
 7.5% of cases are affected in Thoduvali
 5% of cases are affected in Increased Viyarvai

 Interpretation of Malam
 Yellow colouration of the malam is noted 100% of cases
 Irukal present in 80% of cases
 Bulky of stool is noted in 5% of cases
158
 Interpretation of Mooththiram

 Neerkkuri
 Yellow colouration of urine is present in 97.5% of cases
 Red colouration of urine is present in 2.5% of cases.
 Nurai is present in 12. 5% of cases
 Manam is present in 12. 5% of cases
 Enjal is present in 5% of cases

 Neikkuri
 Mothiraththil Muththu shape is present in 42.5% of cases
 Mothiraththil Aravam shape is present in 27.5% of cases
 Mothiram shape is present in 10 % of cases
 Aravam shape is present in 7.5% of cases
 Muththu shape is present in 5% of cases
 Muththil Aravam shape is present in 5% of cases
 Aravi Mothiram shape is present in 2.5% of cases

 Interpretation of Naadi

 Kaalam
 45% of cases naadi are present in munpani kaalam
 32.5% of cases naadi are present in pinpani kaalam
 10% of cases naadi are present in Ilavenit kaalam
 5% of cases naadi are present in Kaar kaalam.
 5% of cases naadi are present in Koothir kaalam
 2.5% of cases naadi are present in Mudhuvenit kaalam

 Thesam
 100% of cases naadi are present in Veppa Kaalam

159
 Udal vanmai
 57.5% of cases udal vanmai is Iyalpu
 35% of cases udal vanmai is Melivu
 7.5% of cases udal vanmai is Valivu
 Nadiyin vanmai
 77.5% of cases are present in Vanmai
 22.5% of cases are present in Menmai

 Naadi nadai
 Azhalvali nadi is noted in 57.5% of cases
 Valiazhal nadi is noted in 30% of cases
 Azhaliyam nadi is noted in 10 % of cases
 Iyavali nadi is noted in 2.5% of cases

 Interpretation of Haemoglobin
 100% of cases are present in Hb below 10g/dl

 Interpretation of Peripheral smear

 47.5% of cases are present in Hypochromic microcytic Anaemia :
( Vatham -7.5%, Piththam37.5%, Kabham – 2.5%)
 42.5% of cases are present in Iron deficiency Anaemia :
(Vatham – 5%, Piththam 35%, Kabham 2.5%)
 10% of cases are present in other type (Iron and B 12 deficiency) of Anaemia.:
(Piththam 7.5%, Kabham 2.5%

 Interpretation of Blood grouping

 45% of cases are affected in B group : (Vatham- 5%, Piththam – 40%)
 22.5% of cases are affected in O group :( Piththam – 17.5%, Kabam -5%)
 17.5% of cases are affected in A/A1 group : ( vatham -5%, Piththam – 10%,
Kabham – 2.5%)
 15% of cases are affected in AB group : (Vatham -2.5%, Piththam -12.5% )
 97.5% of cases are present in Rh Positive
 2.5% of cases are present in Rh Negative.

160
CONCLUTION
The aim of study is to evaluate the predominant Siddha parameters
observed in Paandu noi and compare with Modern parameters.

 DIET :- Paandu noi is prominently found occur in 33 cases in mixed diet – By

author observed that diet maybe the major cause to the Paandu noi.

 NILAM :-
 Panndu noi is prominently afected 24 cases in Mullai nilam. In living peoples are
mostly affected in Piththa noi. By author observed this nilam is maybe the largest
occurance of piththa type of paandu noi.
 5 cases are affected in Neithal nilam. In neithal nilam mostly vatha types of
paandu noi observed.
 3 cases is affected in Kurinchi nilam. In Kurinchi nilam mostly kapha types of
paandu noi observed.

 SIGN AND SYMPTOMS :- By author observed in

 32 cases are sign and symptoms are correlated in the piththa paandu noi ,
 5 cases are sign and symptoms are correlated in the Vathapaandu noi
 3 cases are sign and symptoms are correlated in the Kaphapaandu noi.

 ENVAGAI THERVUGAL :- By author observed in

1. Naa – Niram in
 32 cases are veluppu niram is correlate the Kaphapaandu
 04 cases are manjal niram is correlate the Piththa paandu.
 04 cases are Karuppu niram is correlate the Vatha paandu.

Naa – Suvai in

 32 cases Kaippu suvai is present. It is correlated with Piththa Paandu.

 5 cases Pulippu suvai is present . It is correlated with Vaatha Paandu
 3 cases Uppu suvai is present . It is correlated with Kapha Paandu

161
2. NIRAM :- By author observed in,
 33 cases are present with veluppu niram. It is correlated with Kapha paandu
 4 cases are present with manjal niram. It is correlated with Piththa paandu
 3 cases are present with Karuppu niram. It is correlated with Vatha paandu

3. MOZHI- By author observed in,

 24 cases are having in Uraththa oli. It is correlated with Piththa paandu noi.
 09 cases are having in Sama oli. It is correlated with Vaatha paandu noi
 07 cases are having in Thaalntha oli. It is correlated with Kapha paandu noi

4. VIZHI - By author observed in,

 33 cases are present in Veluppu niram. It is correlated with Kapha paandu noi.
 06 cases are present in Manjal niram. It is correlated with Piththa paandu noi.
 01 case is present in Sivappu niram. It is correlated with Vaatha paandu noi.

5. ISPARISAM - By author observed in,

 24 cases are having in Mithaveppam. It is correlate with Piththa paandu noi.
 16 cases are having in Veppam. It is correlate with Vaatha paandu noi.

6. MALAM - By author observed in,

 40 cases are present in Manjal nira malam. It is correlate with Piththa paandu noi.

7. MOOTHTHIRAM
 NEERKKURI - By author observed in,
 39 cases are present in Manjal niram. It is correlated with the Piththa paandu noi.
 01 case is present in Sivappu niram. It is correlated with the Piththa paandu noi.

 NEIKKURI - By author observed in,

 17 cases are found in Mothiraththil Muththu, 11 cases are present in Mothiraththil
Aravam and 04 cases are present in Mothiram. There are correlated with the
Piththa paandu noi.
 03 cases are present in Aravam and 01 cases are present in Aravil Mothiram.
There are correlated with the Vaatha paandu noi.

162
 02 cases are present in Muththu and 02 cases are present in Muththil Aravam.
There are correlated with the Kapha paandu noi.

8. NAADI - By author observed in,

 23 cases are present in Azhal Vali and 12 cases are present in Vali azhal. There
are correlated with the Piththa/ Vaath paandu noi.
 4 cases are present in Azhal iyam. It is correlated with the Piththa /Kapha Paandu
noi.
 01 case is present in Iya vali. It is correlated with the Kapha/ Vaatha paandu noi

 UDAL THATHUKKAL - By author observed in,

 40 cases are affected in Saaram and Senneer. There are the causes of Paandu noi.

 MANIKKADAI NOOL - By author observed in,

 10 cases are present in 7 ¼ viratkadai- By author correlated these cases in Paandu
noi.

 PERIPHERAL SMEAR- By author observed in,

 19 cases are correlated in Hypochromic microcytic anaemia. There are present in
Piththa paandu noi -15, Vaatha paandu noi – 03, Kapha paandunio -01)
 17 cases are correlated in Iron deficiency anaemia. There are correlate in the
Piththa paandu noi- 14, Vaatha paandu noi- 02, Kapha paandu noi- 01
 04 cases are correlated in Iron and B12 deficiency anaemia. There are correlated
in Piththa paandu noi – 03,Kapha paandu noi-01

 BLOOD GROUPING- By author observed in,

 18 cases are present in B positive . It is including Piththa paandu noi-16 and
Vaatha paandu noi – 02. By author observed paandu noi is mostly affected in B
positive blood group person.
 39 cases are present in Rh possitive. By author observed paandu noi is mostly
affected in Rh positive person

163
 BY AUTHOR OBSERVED IN THIS OVERALL STUDY

The following results are observed in Food habbit, Nilam, Sign and
symptoms, Envagaitheervugal, Udal thathukkal, Manikkadainool , Peripheral
smear , Blood grouping and other significant datas are help in taking the final
conclution in this clinical study.

 32 CASES OBSERVED IN PITHTHA PAANDU NOI

 05 CASES ARE OBSERVED IN VAATHA PAANDU NOI
 03 CASES ARE OBSERVED IN KAPHA PAANDU NOI.

164
6.0 SIDDHA TREATMENT OF ANAEMIA

kUj;Jtg; gupfhuk;

rpj;j kUj;Jtj;jpy; Neha;fF

; kl;Lk; kUj;Jtkd;wp mjidtuhJ
jLf;fTk; fhafw;gkhfTk; kUe;Jfs; gad;gLk; ,jidNah fhg;G > ePf;fk;>
epiwT vd;gdthFk;.

rpj;jkUj;Jt Kiwg;gb xt;nthU fUTk; cUthFk; nghOJ mjpy;

Vw;gLk; rpy khWjypdhy; fUtpNy NehAz;lhfpwJ.

Kf;Fw;wj;jpy; Vw;gLk; NtWghLfs; - czT>gof;f tof;fq;fs;> tho;f;if

topKiw fhuzkhf Neha; Vw;gLk;.

“ Neha; ehb Neha;Kjy; ehbaJ jzpf;fk;

tha;ehb tha;g;gr; nray;”

- jpUf;Fws;

,jdhy; Neha; tuf;$ba topfisAk; Neha;f; fhuzq;fisAk; mwptJ

Kf;fpakhFk;.

“ cw;whdsTk; gpzpasT; fhyKk;

fw;whd; fUjp;r; nray;”

- jpUf;Fws;

Nehapdd; mile;j Fw;w NtWghLfspd; kpFjy; msitAk; mjdhy;

NehAw;whd; ngw;w Nehapd; msitAk; mwpe;j gp;d; Nehapd; fhy msit
mwpe;J rpe;jpj;J jFe;j kUj;Jtk; GuptJ mtrpak;.

6.1 kUj;Jt topKiwfs;

Nflile;j Kf;Fw;wk; thAf;fs;> ,uj;jjhJ> ,jid rkg;gLj;Jk;

kUe;Jfshf ,Uf;f Ntz;Lk;. ehk; nfhLf;Fk; kUe;JfshdJ ,uQ;rf
gpj;jj;ijg; rkg;gLj;jp ,uj;j jhJit jd; ,ay;ghd Ntiyfs; nra;tjhf
khw;w Ntz;Lk;.

“tpNur;rdj;jhy; thjk; jhOk;

tkdj;jhy; gpj;je; jhOk;

erpa mQ;rdj;jhy; fge; jhOk;”

165
 mjpfupj;j gpj;jj;ij jd;dpiyg;gLj;j the;jp kUj;Jtk; nra;jy; Ntz;Lk;.
ghz;L Nehapy; Nehahsp NrhHthfTk;> jsHTlDk; ,Ug;gjhy; the;jp Kiw
kUj;JtkhdJ nfhLg;gjpy;iy.

,uj;j jhJit mjpfupf;f mak; rhHe;j kUe;Jfis toq;f Ntz;Lk;.

Neha;ff
; hd fhuzq;fisj; jtpHf;f Ntz;Lk;.

grpj;jPia mjpfupf;fr; nra;Ak; kUe;Jfis toq;f Ntz;Lk;.

gj;jpak; vspjhf ,Uf;f Ntz;Lk;.

mjpf rj;Js;s czit cl;nfhs;s nra;a Ntz;Lk;.

LINE OF TREATMENT
 ghz;L Nehapw;F kUj;JtkhdJ> FUjpapd; ePHg;ghfj;ijf; Fiwf;ff;
$baJk; gpj;jkhfpa jplg;nghUl;fis $l;lf;$baJkhd czitAk;
kUe;JfisAk; nfhLf;fNtz;Lk;.
 jd;epiy khWgl;l Fw;wq;fis jd;epiyg;gLjJtjw;fhf fopr;ry;
kUe;Jfisf; nfhLf;f Ntz;Lk;. gpd;G grpj;jPiaj; J}z;Lk; kUe;JfNshL>
FUjpapd; td;ikiag; ngUf;fNtz;ba kUe;JfisAk; nfhLf;f Ntz;Lk;.
 rpWePiuf; fopf;ff; $baJk;> vUf;fl;il jPHf;ff; $baJkhd FbePH> gw;gk;>
nre;J}uq;fis toq;f Ntz;Lk;.
 nfhl;ilj; jpuhl;ir NrHe;j fopr;ry; kUe;Jfs;> mfj;jpf; fPiuf;FbePH>
epyhthiu NrHe;j FbePH> Nghd;w fopr;ry; FbePHfisf; nfhLj;j gp;d;G
grpj;jPiaj; J}z;Ltjw;fhd nghb tiffisj; Jiahff;
nfhz;L ,Uk;gpidg; gad;gLj;jp jahupf;fg;gl;l kUe;jfisg; gad;gLj;jp
kUj;Jtk; nra;jy; Ntz;Lk;
 khJis kzg;ghF> rpwe;jJ
 gpuhzhahkk;> rh;thq;fhrdk; Nghd;w Nahfhrdq;fs; > gpuzhahkk; vDk;
%r;Rg;gapw;rAk; rpwe;j ngWNgiwf; nfhLf;Fk;.

166
 DIETARY REGIMEN

czT

 “ khWghby;yh cz;b kWj;Jz;zpd;

; ”
CWgh by;iyA aph;fF

- jpUf;Fws;
 ehk; cl;nfhs;Sk; czthdJ cliy td;ikg;gLj;jf;$bajhfTk;>
cliy fha fw;gkhf khw;wf;$bajhfTk; ,Uf;f Ntz;Lk;.
 Neha; njhlf;fj;jpy; grpiaj;J}z;lf;$baJk;> clypd; FUjpia ngUf;ff;
$baJkhd czTg; nghUl;fis ngupJk; ifahsy; Ntz;Lk;.
 czTk; vspjpy; nrupf;ff;$bajhfNt ,Uj;jy; Ntz;Lk;.

fPiufs;

fuprhiy> nghd;dhq;fhzp> mwf;fPiu> rpWfPiu> KUf;fq;fPiu> kzj;jf;fhsp

fha;fwpfs;

fj;jupg;gpQ;R> Mthiu gpQ;R> KUf;if gpQ;R> thio fr;ry;

goq;fs;

NguPr;rk; gok;> Njhlk;gok;> jpuhl;ir> Mg;gps;> mj;jpg;gok;> ney;yp> khJsk;

gok;

mirt tiffs;

nts;shl;Lf;fwp> Ml;L<uy;> Ml;L vYk;;G> fhil> nfsjhup> cs;shd;>

cLk;G> Cdpd; urk;. vd;gd FUjpiag;gyg;gLj;jg; gad;gLk;.

NkYk;

gdq;fw;fz;L> fly; kPd;> fly;rhHe;j czTg;nghUl;fs;> rpwe;jJ.

ghz;L Neha;f;F toq;fg;gLk; %ypiffs;

“ nrg;GfpNwd; ghz;L fhkhiy Nrhif

jPHf;fpd;w ruf;F tha;tpsq; fe;jhk;

xg;gpy;yh $tpis NtH ej;ijr;#up

Crpky;yp kUl;fpoq;F ey;yNtis

xg;gpy;yhky; %ypfupg;ghd; r%yk;

167
cuf;F kz;^Nu kak; Riuf; nfhOe;J

nrg;ghk;gpj; jhisg;gw;gk; Gspak;gl;il

rpWgPis jha;f nfhl;lhd; rpWfPiu Nth;

NtnuhL ntz;fhuk; G+idf; fhyp

tpj;J ,sePh; Kj;J fPo;fha; ney;yp

NtnuhL G+te;jpg; gok; muj;ij

nts;isf; fhf;fz NtH fhl;lh kzf;F

NtNuhL G+kp rH;f;fiu fpoq;F

nts;shl;bd; ePH ghy; rhuhiz NtHf;fs;sp

NtnuhL [ykQ;rupr; nre;Juk;

kpsF jf;fhspapiy ney;ypapd; NtH

ney;yp NtH jpidf; fQ;rp %Rky;yp

ePH Ks;sp r%yk; G+turk; gl;il

nfhy;yd; Nfhit Aila r%yk; tl;lf;

fpYfpYg;ig thioePh; thioAl;b

tpy;t ,iy ghjpupNtH Fsj;Jg;ghiy

NtnuhL NfhkpaKk; m];tfe;jp

fy;ahz fug;ghd; jf;NfhyKk; gpuk;kp

fhuhd; jpupfLF ghiy FwpQ;rh

FUQ;rh ehfzk; GspapDiyap NdhL

$wpa ,t;tk;igj; njl;L ruf;Fk;

ngUe; njhy;iyahk; ghz;L Nrhif tPf;fk;

gpj;jj; jhnyLj;j njhU Nehia nay;yhk;

ngUe; njhiyapNyhl;L tpf;Fk;

gjhHj;j Fz tpsf;Fk;”

- itj;jpa rh];jpuk;

168
nghUs;:

tha;tplq;fk;> ej;ijr;#up> ey;yNtis> fupg;ghd; r%yk;>

Riuf;nfhOe;J> rpWgPio> rpW fPiuNtH> G+idf;fhyp tpij> ,sePH>
fPohney;yp> muj;ij> nts;isf; fhf;fzNtH> fhl;lhkzf;F NtH> G+kp
rHf;fiuf; fpoq;F> rhuizNtH> ney;yp> jpidf;fQ;rp> ePH Ks;sp r%yk;>
G+turk; gl;il> nfhy;yd;Nfhit> tl;lf; fpYfpYg;ig> thioePH>
tpy;t ,iy> ghjpupNtH> m];tfe;jp> jf;Nfhyk;> gpuk;kp. jpupfLF

169
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51
52
 PG NOINADAL DEPARTMENT
GOVERNMENT SIDDHA MEDICAL COLLEGE PALAYAMKOTTAI .
A CLINICAL STUDY ON DIAGNOSTIC METHODOLOGY OF PAANDU THROUGH SIDDHA
PARAMETERS
1. O.P.NO :……………………………………
2. S.No …………………………………….
3. Date …………………………………….
4. Name …………………………………….
5. Age …………………………………….
6. Sex …………………………………….

RESULT
1. Diagnosis …………………………….
2. Neikkuri ……………………………...
3. Nadi ……………………………...
4. Manikkadai Nool ……………………………..
5. Blood Group ……………………………
6. Peripheral Smear …………………………….

Signature of the Assistant Medical Officer ………………………………………

Signature of the Guide …………………………………………

 PG NOINADAL DEPARTMENT
GOVERNMENT SIDDHA MEDICAL COLLEGE, PALAYAMKOTTAI .
“A CLINICAL STUDY ON DIAGNOSTIC METHODOLOGY OF PANDU THROUGH SIDDHA
PARAMETERS”
FORM I
SCREENING AND SELECTION PROFORMA
1. O.P.NO :……………………………………
2. S.No …………………………………….
3. Date …………………………………….
4. Name …………………………………….
5. Age …………………………………….
6. Sex …………………………………….
7. Religion …………………………………….
8. Occupation …………………………………….
9. Income …………………………………….
10. Address …………………………………….
11. Contact No …………………………………….
12. Email ID ………………………………….....

 CRITERIA FOR INCLUTION

 Age 40 years to 65 years : Yes No
 Gender Male and Female : Yes No
 Haemoglobin <10g/dl : Yes No
 Total RBC <4.0 million/ mm3 : Yes No
 PCV < 30% : Yes No
 MCV< 82 fl : Yes No
 MCH < 80 pg : Yes No
 MCHC< 34% : Yes No
 Peripheral smear ( show) : Yes No
 CRITERIA FOR EXCLUTION
 Age below 39 years : Yes No
 Age above 65 years : Yes No
 PG NOINADAL DEPARTMENT
GOVERNMENT SIDDHA MEDICAL COLLEGE PALAYAMKOTTAI .
A CLINICAL STUDY ON DIAGNOSTIC METHODOLOGY OF PAANDU THROUGH SIDDHA
PARAMETERS
FORM I - A
PROFORMA
01. O.P.NO :……………………………………
02. S.No …………………………………….
03. Date …………………………………….
04. Name …………………………………….
05. Age …………………………………….
06. Sex …………………………………….
07. Religion …………………………………….
08. Educational status
I. Illiterat II. Literate III. Student IV.Grauate/Post graduate
09. Occupation …………………………………….
10. Income …………………………………….
11. Address …………………………………….
12. Contact No …………………………………….
13. Diagnosis …………………………………….
14. Complaints and duration …………………………………….………………….

14. History of present illness: ………………………………………………………..

…………………………………….…………………………………….………………………
…………….…………………………………….………………………………
15. Past History
…………………………………….…………………………………………………….
…………………………………….…………………………………….………………………
16. Family History …………………………………….…………………………
17. Personal History …………………………………….………………………….
…………………………………………………………………………………………
18. FOOD AND HABITS
a. Food Veg NonVeg v Mixed
Tea Coffee Smoking Alcohol
Betelnut Tobacco Yoga Others ……

19. General etiology for Paandu

a. Poor Nutritional Diet YES NO
b. Alteration in cooking of food YES NO
c. Alcoholism YES NO
d. Gastro Intestinal Tract diseases YES NO
e. Medication YES NO
f. Malignancy YES NO

20. General clinical symptoms of Paandu ABSENT PRESENT

a. Uthadu orankalil vediththal, Vaaippun
(stomatitis)
b. Kan vezuththal (pallor of the eyes)
c. Uthadu vezuththal (pallor of the lips)
d. Mukam Vezuththal(pallor of the face)
e. Naakku vezuththal ( Pallor of the Tongue)
f. Thol varadchi mattum vezuththal
a. (Pallor and dryness of the skin)
g. Pasiyinmai(Anorexia)
h. Padapadappu (Palpitation)
i. Sompal(Lassitute)
j. Sorvu, Mayakkam ( Tiredness)
k. Ithaya nadai Kuraithal(Bradycardia)
l. Velayinpothu moochchuththinaral
( Dyspnoea on exertion)
m. Vizhi pithukkam (Protrusion of eye balls)
n. Kanukkaal veekkam (Angle odema)
o. Thuruththi nigar oli ( Added heart sound)
 21. GENERAL EXAMINATION
a. Udal veppanilai ( Temperature) .………………………………
b. Nadiththudippu enn (Pulse rate) ……………………………….
c. Irudhaya thudippu enn (Heart rate) ……………………………….
d. Suvasa enn (Respiratory rate) ……………………………….
e. Kuruthi azuththam (Blood pressure) ……………………………….
f. Udal veluththkkanal( Pallor) .………………………………
g. Udal manchaliththal (Jaundice) ………………………………
h. Neelam paariththal (Cyanosis) ………………………………
i. Ninaneerkozha veekkam (Lymphadinopathy) ..…………………………….
j. Kanukkal veekkam( Pedal oedema) ………………………………
k. Nakakkan thadippu (Clubbing) ………………………………
l. Kandhara nalaththudippu (Jugular venous pulse) ……………………………….
m. Weight …………………………….....
n. Height ……………………………….
o. BMI ……………………………….

22. VITAL ORGANS EXAMINATION

1. NORMAL 2. AFFECT
a. Iraipai (Stomach) v
b. Kalleral (Liver) v

c. Manneral (Spleen)
d. Puppusam (Lungs)
e. irudhayam( Heart)
f. Pirukkam(Kidney)
g. Moolai (Brain)

23. SIDDHA SYSTEM OF EXAMINATION

A. IYMPORIKAL/IYPULANKAL 1. NORMAL 2.AFFECTED
a. Mei/Ooru
b. Vaai – Suvai
 c. Kan – Ozli
d. Mooku – Naatram
e. Sevi – Osai
B. KANMENTHIRIYANGAL/ KANMAVIDAYANGAL
NORMAL AFFECTED
a. Kai – Thaanam v
b. Kaal – Kamanam
c. Vaai – Vasanam
d. Eruvaai – Visarkkam
e. Karuvai – Aanantham
C. GUNAM

Saththuvam Rasatham Thamasam

D. KOSAM 1. NORMAL 2. AFFECTED

a. Annamaya (Udarththathukkal) v
b. Pranamayakosam (Pranan, Kanmenthiiyam)
c. Manomaya Kosam ( Manam, Gnanenthiriyam)
d. Vinganamaya Kosam ( Puththi, Gnanenthiriyam)
e. Ananthamaya Kosam ( Pranan, Suzuththi)
E. UYIRTHATHUKKAL
a. VALI NORMAL AFFECTED
a. Pranan(Uyirkkal)
b. Abanan (Kelnokkunkaal)
c. Samanan (Nadukkal)
d. Udanan (Melnokkunkal)
v
e. Viyanan (Paravukal)
f. Naagan
g. Koorman
h. Kirukaran
i. Thevathaththan
j. Thananjeyan
 b. AZHAL NORMAL AFFECTED
a. Akkanal (Anila piththam)
b. Vannayeri ( Ranjaka piththam)
c. Ulloliththee ( Prasaka piththam)
d. Nokkuazhal (Aalosaka piththam)
e. Aatralangi ( Saathaka piththam)

c. IYAM NORMAL AFFECTED

a. Ali Iyam (Avalambagam)
b. Neerppi Iyam (Kilethagam)
c. Suvaikaan Iyam (Pothagam)
d. Niraivu Iyam (Tharppagam)
e. Ondri Iyam (Santhigam)

G. UDAL THATHUKKAL NORMAL AFFECTED

a. Saaram
b. Senneer
c. Oon
d. Kozhuppu
e. Enbu
f. Moolai
g. Sukkilam/ Suronitham

24. SIGN AND SYMPTOMS IN VARIOUS TYPES OF PAANDU

VATHA PAANDU YES NO
a. Vayiru kaikaalkalil vali
b. ( Pain in the extremities and abdomen)
c. Kankalaichchuttiya veekkam (Oedema of the eye ball)
d. Muka veekkam ( Oedema of the face)
e. Kaikalil veekkam ( Oedema of the arm)
f. Udal veluththal ( Pallor of the body)
 g. Sompal (Lassitude)
h. Moochchuththinaral (Dyspnoea)
i. Vaanthi ( Vomiting)
j. Vikkal (Hiccough) v v
k. Athikariththa vaai neerooral ( Excessive salaivation) v v

PITHA PAANDU YES NO

a. Udal manchaliththal (Yellowish colouration of the body)
b. Kann manjaliththal ((Yellowish colouration of the eye)
c. Nail manjaliththal ((Yellowish colouration of the nail) v v
v v
d. Siruneer manchliththal (Yellowish discolouration of the urine)
e. Malam manchalliththal (Yellowish discolouration of the stool)
f. Moozai keddu puththi maaruthal
g. ( Mood swing loss of intelligence)
h. Malam vezuththal ( Pallor of the stool)
i. Udal arippu ( Body itching)
j. Sourvu (Tiredness)
k. Marathi (Memory loss)
l. Moochchuththinaral ( Dyspnoea)
m. Thalai suttal ( Giddiness)
n. Sompal ( Lassitude)
o. Vaai kasappu ( Biiter in taste) c c
v v
p. Udal melithal ( Emaciation)
c c
v v
v v
KAPA PAANDU YES
z NOz
a. Thol minuminuppu ( Shining of skin) z z
z z
b. Vayiru uppal ( Abdomenal flatulence) z z
z z
c. Paatha veekkam ( Oedma of the feet) z v vz
d. Kaikalin pinpura veekkam ( Oedema of the dorsum of the hand)
e. Vayiru veekkam ( Abdominal swelling) v
v
f. Naa veekkam ( Swelling of tongue)
g. Sompal ( Lassitude)
 h. Thalai suttal ( Giddiness)
i. Thaazhntha oli (Huskey voice)
j. Kaan vezhuththal ( Pallor of the Eye)
k. Mukam vezhuththal ( Pallor of the Face)
l. Siruneer vezhuththal ( Pallor of the urine) v
m. Mazham vezhuththal ( Pallor of the faeces) v

n. Athi viyarvai ( Excessive sweating)

o. Kankalil kuzhirchchi (Chillness of eyes)
p. Vilaap pakuthikalil vali ( Thoracic pai)
v v
q. Udal muttum veekkam ( Anasarca)
r. Nenjil vali ( Chest pain)

VISHA PAANDU Yes No

a. Udal Veluththal (Pallor of the body)
b. Miku suram (High Fever )
c. Vaanthi (Vomitting)
d. Vikkal (Hic-cough)
e. Irumal (Cough)
f. Puththipiralal (Hallucination)
g. Udal veenkal ( General oedema)
h. Pasiyinmai, Arosakam (increased body heat)
MIRUTHTHIKA PAANDU
a. Malam, mooththiram manchaliththal
1. (Yellow colouration urine, stool)
b. Seriyamai ( Indigestion)
c. Vayiru upputhal (Flatulence) v
d. Vaanthi ( Vomitting)
v
e. Udal muzhuvathum veenkuthal ( General oedema)
f. Iraththam, Kirumi, Kozhai kalantha kazhichchal
( Bacillary dyesentary)
 2. STATE OF PAANDU
Vatha Paandu PithaPaandu Kapa paandu
Miruththika Paandu

25. NOI UTTRA KAALAM

a. Kaarkalam (Avani, Purattasi)
b. Koothirkaalam( Ippasi, Kaarththikai)
c. Munpanikkalm (Maarkazhi, Thai)
d. Pinpanikkaalam (Maasi, Panguni)
e. Illavenirkaalam (Chiththirai, Vaikasi)
f. Mudthuvenirkalam (Aani,Aadi)

26. NOI UTRA NILAM

Kurinji Mullai Marudham Neidhal Paalai

27. ENVAGAI THERVUGAL

A. NAKKU
a. Maa padinthiruththal Absent Present
b. Niram Karuppu Manjal Veluppu
others …………..
c. Suvai Inippu Uppu Kaarppu Pulippu . Kaippu
Thuvarppu
d. vedippu Absent Present
e. Vaai neer ooral Normal Excess Scanty Absent
f. Naakkupun Absent Present
B. NIRAM Karuppu Manjal Veluppu Maniram
C. MOZHI Sama oli ….. Uratha oli Thaazhntha oli
D. VIZHI
a. Niram Karuppu…. Manjal Veluppu Sivappu
b. Kanneer Normal Abnormal
c. Erachchal Absent Present
 d. Peelai seruthal Absent Present
e. paarvai Normal Abnormal
E. ISPARISAM
a. Veppam Midhaveppam Veppam Thatpanam
b. Viyarvai Normal Increased Reduced
c. Thodu vali Absent Present
F. MALAM
a. Niram Karuppu Manjal Veluppu
b. Thanmai Ilakal Irukal Thin Bulky
c. Alavu Normal Increased Decreased
d. Kalichchal Absent v Present
e. seetham Absent v Present v
f. Venmai Absent v Present v
g. Raktha kalichchal Absent v Present v
h. Thadavai (Frequency) Day v Night v
G. MOOTHTHIRAM (Siruneer)
NEERKKURI
a) Niram Venmai v Sivappu v Manjal v Others v
b) Manam Absent v Precent v
c) Nurai Present v Absent v
d) Edai- kanam Present v Absent v
e) Enjal- Deposit Present v Absent v
f) Thadavai Day v Night v

NEIKKURI
a. Aravam v Moththiram v Muththu v
b. Aravil mothiram Aravil muththu v Mothiraththil Aravam v
v
c. Mothiraththil muththu v Muththil Aravam v Muththil Aravam v
d. Muththil mothiram v Asaththiyam v Melenna paraval v
H. NAADI
a. Kaalam v Kaarkaalam v Koothirkaalam v Munpanikaalam v
b. Pinpanikaalam v Ilavenirkaalam v Mudhuvenirkaalam
v
c. Desam v
Kulir v Veppam v
d. Udal Vanmai v Iyyalpu v Valivu v Melivu v
e. Naadyin Vanmai v Vanmai v Menmai v
f. NaadiNadai v Vali v Azhal v Iyam v
Valiazhal v
v

g. Valiiyam v Azhalvali v Azhaliyam v Iyavali v Iyaazhal v

Sanni v

28. MANIKKADAINOOL

29. RASI …………………………………….

30. NADSATHTHIRAM …………………………………....
INVESTIGATION
31. BLOOD
a. W.B.C …………………………………….
b. E.S.R …………………………………….
c. BLOOD SUGAR : F/PP/R …………………………………….
d. BLOOD UREA …………………………………….
e. SERUM CHOLESTEROL ……………………………………

32. INVESTIGATIONS FOR ANAEMIA

i. R.B.C …………………………………….
ii. D.C Neutrophill …… Lymphocyte……… Eosinophil……. Basophill…… monocyte…….
a. Haemoglobin :- …………………………………….
b. Haematocrit (PCV) :- …………………………………….
c. MCV :- …………………………………….
d. MCH :- …………………………………….
e. MCHC :- …………………………………….
f. PERIPHERAL SMEAR :- …………………………………….
g. BLOOD GROUPING :- …………………………………….

33. URINE
a. ALBUMIN :- …………………………………….
b. SUGAR :- …………………………………….
c. DEPOSITES :-……………………………………...
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 GOVT SIDDHA HOSPITAL – PALAYAMKOTTAI DEPARTMENT OF
NOINAADAL THROUGH SIDDHA PARAMETERS

FORM IV A

INFORMED WRITTEN CONSERN FORM

I ………………………………………..exercsing my free power of choice, hereby give

my consent to be included as a subject in the diagnostic trial entitled A study on “PAANDU” . I
will be required to undergo all routine examinations. I may be asked to give urine and blood
samples during the study.

I have been informed about the study to my satisfaction by the attending investigator and
the purpose of this trial and the nature of study and the laboratory investigations. I also give my
consent to publish my urine sample photographs in scientific conference and reputed scientific
journals for the betterments of clinical research

I am also aware of my right to OPT out of the trial at any time during the course of the trial
without having to give the reason for doing so.

Signature/ thumb impression of the patient

Date :

Name of the patient :

Signature of the investigator :

Date :

Head of the Department :

Date :
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