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From: Dr. MINU. P. Post Graduate Student, Post Graduate Dept. of Repertory and Case taking, DBHP Sabah’s. Dr. B. D. Jatti Homoeopathic Medical College,Hospital & P.G. Research Center, D.C. Compound, Dharwad-580001.
To: The RegistrarRajiv Gandhi University of Health Sciences, Karnataka, Bangalore.
Through:
The Principal DBHP Sabha’s. Dr. B. D. Jatti Homoeopathic Medical College, Hospital & P.G. Research Center, Dharwad-580 001.
Respected Sir,
Subject: Submission of Completed Proforma of Synopsis for Registration of Subject for Dissertation.
I request you to kindly register the below mentioned subject against my name for the submission of dissertation to the Rajiv Gandhi University of Health Sciences, Bangalore in partial fulfillment for the award of the degree of M.D. (Homoeopathy) in Repertory.
Title of Dissertation:
“A COMPARATIVE STUDY ON LOGICO-UTILITARIAN REPERTORIES AND CLINICAL REPERTORIES IN THE
MANAGEMENT OF TYPE 2 DIABETES MELLITUS”
I am herewith enclosing completed proforma of synopsis for registration of subject for dissertation.
Thanking you,
Place: Dharwad Yours faithfully Date:
(Dr. MINU. P)
“A COMPARATIVE STUDY ON LOGICO-UTILITARIAN REPERTORIES AND CLINICAL REPERTORIES IN THE
MANAGEMENT OF TYPE 2 DIABETES MELLITUS”
SYNOPSIS
Submitted to
RAJIV GANDHI UNIVERSITY OF HEALTH SCIENCES KARNATAKA, BANGALORE,
BY
Dr. MINU. P
ThroughDPHP’s
DR. B. D. JATTI HOMOEOPATHIC MEDICAL COLLEGE, HOSPITAL & P.G.
RESEARCH CENTER, D.C. COMPOUND, DHARWAD-580001.
(KARNATAKA)
In partial fulfillment of requirement for the
DOCTOR OF MEDICINE (HOMOEOPATHY)
HOMOEOPATHIC REPERTORY
Under the valuable guidance of
DR. SUDHANSU SEKHAR MOHARANA
PROFESSOR
Dept. of Hom. Repertory. DR. B. D. JATTI HOMOEOPATHIC MEDICAL COLLEGE, HOSPITAL & P.G.
RESEARCH CENTER, D.C. COMPOUND, DHARWAD-580001.
(KARNATAKA)
RAJIV GANDHI UNIVERSITY OF HEALTH SCIENCES, KARNATAKA, BANGALORE.
Annexure-II
REGISTRATION OF SUBJECT FOR DISSERTATION
1. NAME OF CANDIDATE & ADDRESS
Dr. MINU. P. Post Graduate Student,Post Graduate Dept of Repertory and Case taking,Dr. B. D. Jatti Homoeopathic Medical College, Hospital & P.G. Research Center,Dharwad-580001
PERMANENT ADDRESS Dr. MINU. P. D/o. P. Gangadharan58/1, “Sree Ganga”J.R. Colony, New ThippasandraBANGALORE-560075
2.NAME OF THE INSTITUTION
D.B.H.P. Sabha’sDr. B. D. Jatti Homoeopathic Medical College, Hospital & P.G. Research Center, D. C. Compound, Dharwad-580001
3.COURSE OF STUDY AND SUBJECT
M. D. (HOMOEOPATHY) REPERTORY
4.DATE OF ADMISSION TO COURSE 07-07-2010
5.TITLE OF THE TOPIC “A COMPARATIVE STUDY ON LOGICO-
UTILITARIAN REPERTORIES AND CLINICAL REPERTORIES IN THE
MANAGEMENT OF TYPE 2 DIABETES MELLITUS”
6 BRIEF RESUME OF THE INTENDED WORK 6.1 NEED FOR THE STUDY:
In the vast majority of type 2 diabetics the principal abnormality is one
of the reduced insulin sensitivity. However, if insulin secretion is
insufficient to compensate, impaired glucose tolerance or frank
diabetes results. This typically occurs as a result of β cell exhaustion.
Occasionally, insulin sensitivity is normal but insulin production is
reduced (e.g. maturity-onset diabetes of the young [MODY]); diabetes
again results.
The prevalence of type 2 in Britain is around 2.3% type 2 diabetes
occurs in migrant populations to industrialized countries as in Asia and
Afro-Caribbean immigrants to the UK.
Type 2 DM is a multi-factorial disease with genetical and
environmental factors including possible infections. Precipitating
causes like physical or emotional stress. At present there is an
outerageous evidence to say Indians are prone to type 2 diabetes due to
diseased life style rather than genes. Which ultimately harms our
healthy genes and turning them against us.
Insulin, which was discovered by Fedrick Bunting and Charles Best in
1921, Since then it had saved millions of lives all over the world.
Modern medicines contribute immensely and saved millions of people.
Majority of the patients are geriatric, most drugs are metabolized in the
liver. With age the ability of the liver to degrade and is diminished
which leads to more toxicity. Thus the side effect of oral hypoglycemic
agents and the development of Insulin hypersensitivity and resistance
must be taken into consideration. Though insulin therapy is considered
to be live saving, but there are some controversial aspect about the side
effects of insulin therapy. The most common side effects of insulin
therapy is low blood sugar. Other side effects of insulin therapy is
redness, swelling or itching at the site of injection, worsening of
diabetic retinopathy, changes in distribution of body fat
(lipodystrophy), allergic reactions, sodium retention and general body
swelling, a type of chest discomfort, cough and dyspnea. It is also seen
that there is weight gain, lipoatrophy and lipohypertrophy. The side
effects of oral hypoghycemic agents, Hypoglycaemia, allergic reaction,
dilutional hyponatraemia, cholestasis, lactic acidosis, Anorexia,
Nausea, vomiting, diarrhoea, Abdominal fullness, Bloating,
Hypoglycemia (mild), transient visual disturbance, occasionally transits
elevation of liver enzymes, sinusitis, upper respiratory tract infection,
hepatic injury, headache, Anaemia and oedema, malabsorption of vit
B12, and folic acid, muscle pain, weakness, weight again.
Homeopathy has been said to be having much efficacy in treating type
2 Diabetic mellitus because of its systematic analysis and holistic
approach of considering body, mind and disease and with the concept
of individualization and dynamization. One endeavours to treat all the
symptoms at one time and with one drug. The selection of the potency,
the repetition and the time of releasing the remedial force depend upon
an accurate assessment of the pathogenesis as well as the Pathology
and the qualitative assessment of susceptibility and sensitivity. Thus,
all this criteria is considered for an efficient out come in the
management of the case.
Logical utilitarian Repertories have distinctive principles of their own.
Therefore cases have to be selected to fit them with the principles Eg:
Kent’s Repertory. Synthesis repertory, Boenninghausen’s
characteristics materia medica and Repertory by CM Boger etc.
Clinical Repertory have many clinical rubrics under different systems.
Eg. clinical Repertory by Oscar. E. Boericke, clinical Repertory by J.
H. Clarke etc. making treatment of type 2 DM more inclusive.
Kent’s Repertory is rich in rubric of generalities and mind. Synthesis
repertory is rich in ailment from sub-rubric of the mind and rubric of
generals and characteristics particulars. Boger Boenninghausen’s
characteristics and repertory by CM Boger is rich in pathological
generals and clinical rubrics with rich in modalities sensations and
concomitants. Clinical repertory by Oscar. E. Boerick is rich in clinical
rubrics. All the headings are presented under definite captions in the
following order, course, type, location, character of the pain,
concomitants and modalities. Technical names of diseases are
bracketed, thereby assuming a subsidiary place, which is in strict
accord with Homoeopathic requirement. Clinical Repertory by J. H.
Clarke is rich in clinical condition, clinical relationships,
temperaments, dispositions, constitutions and states. Thus clinical,
pathological generals, physical and mental generals are of immense
value in treatment of type 2 DM.
Thus a comparative study on logico-utilitarian repertories and clinical
repertories is undertaken to ascertain the Homoeopathic management of
type 2 Diabetic Mellitus.
Hence, this study is undertaken to determine the comparative efficacy
of logico-utilitarian repertories and clinical repertories.
6.2 REVIEW OF LITERATURE HISTORICAL REVIEW
1. The name diabetes is derived from the Greek word for ‘Syphen’. It is
disease of great antiquity, and some of its salient feature have been
known since the secondary century AD. When Aretaeus described it as
a melting of the flesh and limbs into the urine. Thomas Willis noted
that the urine was ‘wonderfully sweet as if it were inbued with honey
or sugar. Hence the term mellitus, derived from the Latin word for
honey.1 Diabetes is first recorded in English in the form diabetic in a
medical text written around1425. In 1776, Matthew Dobson confirmed
that the sweet taste was because of an excess of a kind of sugar in the
urine and blood of people with diabetes. Diabetes Mellitus appears to
have been a death sentence in the ancient era. Hippocrates makes no
mention of it, which may indicate that he felt the disease was
incurable. Aretaeus did attempt to treat it but could not give a good
prognosis, he commented that “life (with diabetes) is short, disgusting
and painful. Sushruta (6th century BCE) identified diabetes and
classified it as Madhumeha. The further identified it with obesity and
sendentary life style, advising exercises to help “cure it. The ancient
Indians tested for diabetes by observing whether ants were attracted to
persons urine, and called the ailment “Sweet urine, disease”
(Madhumeha). In 1910, sir Edward Albert Sharpey Schofer suggested
that people with diabetes were deficient in a single chemical that was
normally produced by the pancreas–he proposed calling this substance
insulin, from the Latin insula, meaning island, in reference to the
insulin producing islets of langerhans in the pancreas.2
2. Diabetes Mellitus – Comprises a heterogeneous group of metabolic
diseases that are characterized by chronic hyperglycemia and
disturbances in carbohydrate, lipid and protein metabolism. These
diseases result from defects in insulin secretion, insulin action or both.3
3. Classification of Diabetic Mellitus:
Type-1: Insulin dependent diabetic mellitus.
Type-2: Non insulin dependent diabetic mellitus.
Other specific types are due to Genetic defect, Genetic defect of
insulin action, drug induced, viral infection, associated with genetic
syndromes, uncommon forms of immune-mediated diabetes. Excess
endogenous production of hormonal antagonists to insulin.
Gestational diabetes4.
4. Type 2 diabetes mellitus it was previously called maturity onset
diabetes or non insulin dependent diabetes mellitus of obese and non-
obese type.5 There is both reduced sensitivity of tissues to insulin and
impaired regulation of insulin secretion.6
5. The prevalence diabetes mellitus in India is currently reported around
13-15%.7 The overall prevalence of type 2 diabetes in Karnataka was
found to be 16%, among males 18.8% and among females 14.4%.8
Type 2 diabetes is the commonest form of diabetes affecting 5-7%
adults in western society.9 In 2000, according to World Health
Organization, at least 171 million people world wide suffer from
diabetes, or 2.8% of the population.10
6. Type 2 diabetic mellitus is principally a disease of the middle aged and
elderly usually above the aged of 40 years.11
7. Genetic factors are important in the etiology of type 2 diabetes as
shown by marked differences in susceptibility in different ethnic group
and by studies in monozygotic twins where concordance roles for type
2 diabetes approach 100%. Environmental factors, epidemiological
studies provide evidence that type 2 diabetes is associated with
overeating, especially when combined with obesity and under activity.
Obesity probably acts as a diabetogenic factor only in those who are
genetically predisposed to insulin resistance and to β-cell failure. The
risk of developing type 2 diabetes increases tenfold in people with a
body mass index > 30kg/m2.12
8. The basic metabolic defect in type 2 DM is either a delayed insulin
secretion relative to glucose load (impaired insulin secretion) or the
peripheral tissues are unable to respond to insulin (insulin resistance).
Insulin resistance is the most prominent feature of type 2 DM is the
lack of responsiveness of peripheral tissues to insulin, especially of
skeletal muscle and liver. There is increased hepatic synthesis of
glucose. Hyperglycaemia in obesity is related to high levels of free
fatty acids and cytokines. (eg. TNF-l and adiponectin) affect peripheral
tissue sensitivity to respond to insulin. In impaired insulin secretion,
there is failure of β-Cell function to secrete adequate insulin due to the
1) Amylin which forms fibrillar protein deposits in pancreatic islets in
longstanding cases of type 2 DM and also due to
2) Metabolic environment of chronic hyperglycemia surrounding the
islets (glucose toxicity) may paradoxically impair islet cell function.
3) Elevated free fatty acid level (lipotoxicity in these cases may worsen
islet cell function).13
9. CLINICAL FEATURES:
1) Polydipsia, Polyuria, nocturia, weight loss, pruritis vulvae/ balanitis,
impotence.14
2) Weakness, easy fatigability, giddiness, blurring of vision, muscle pain,
cramps and paraesthesias.15
10. DIAGNOSIS OF DIABETES
1. Based on sign and symptoms:
Polyuria, polydipsia, Polyphagia, weight loss, non healing wounds,
recurrent styes, pruritis Vulvae, recurrent urinary tract infections.16
2. Based on Investigation:
Symptoms of diabetes plus causal plasma glucose concentraction
≥ 200 mg/dl(11.1mm ol/c).17
Fasting plasma glucose ≥ 126mgldl (7.0 mmol/c/).17
1 hr post load glucose < 200mg/ dl during an oral glucose tolerance
Test (OGTT).18
11. COMPLICATIONS
- The main metabolic complication in type 2 diabetes mellitus is
Hyperosmolar non-ketonic coma.19 The late complications are Diabetic
retinopathy, Diabetic nephropathy, Diabetic neuropathy, Cardiovascular
diseases,20 Diabetic foot, Diabetic skin – diabetic non healing wounds,
Candidiasis, Diabetic infections21
12. INVESTIGATION
1. Urinalysis: Glycosuria may suggest the presence of diabetes but requires
confirmation with a blood test. Conversely, absence of glycosuria does not
exclude diabetes. The presence of ketones, blood, protein, nitrites and
leucocytes should be noted.
2. Blood glucose: The American Diabetes Association has recently
recommended that the diagnosis of diabetes mellitus should be made on the
basis of a fasting venous plasma glucose level of ≥ 7.0 mmol/L which should
be confirmed on a second occasion. It can also be made however in a
symptomatic patient whose random venous plasma glucose is ≥ 11.1 mmol/L.
3. Others
- Routine blood test: Urea and electrolytes, HbA1c, lipid profile, thyroid
function.
- ECG and chest radiograph (especially in the older patient)
Retinal picture / eye screening.22
13. DIET MANAGEMENT
The importance of diet in the management of diabetes varies with the type of
disease. In non insulin dependent patients not treated with exogenous insulin,
more rigorous adherence to diet is required, since the endogenous insulin
reserve is limited. Such patients cannot respond to the increased demand
produced by excess calories or increased intake of rapidly absorbed
carbohydrate. Medical nutrition therapy for people with diabetes should be
individualized, with consideration given to eating habits and other lifestyle
factors. Nutrition recommendations are then developed to meet treatment
goals and desired outcomes. Flexibility in use of ordinary foods important
patients and families. The first decision is the caloric content of the diet, based
on the need to gain, lose or maintain current weight.23
14) Homoeopathic treatment aims to cure the sickness of the patient by
stimulating the vital dynamic or the power of resistance of the sick person. But
if the power of resistance is weakened by morbific influences of toxic and
parasitic agents also called chronic miasms. Dr. Hahnemann has advised to
remove these obstructions to cure chronic miasms so that no hindrance may
come in the way of cure. Deficiency of insulin is the chief obstruction to cure
diabetes mellitus. Therefore, where insulin deficiency is present and cannot be
stimulated by homoeopathic and specific remedies it should be supplied in
order to remove the obstruction to cure.24
15) In the literature of the new system we found on the one hand report of
decided benefit in the diabetic cases from general and symptomatic treatment,
and on the other certain complete or proximate cures with medicines
presumbly homoeopathic to the essential lesions. Of these hughes gave
attention on phosphoric acid and the salts of uranium. Dr. Stiegele had an
interesting experience with syzgium and arsenicum, where arsenicum was
considered to be antidiabetic.25
16) Urine-Sugar: Acet-ac., all-s., amyl-n., arg-m., ars., benz-ac., Bov., calc.,
calc-p., carb-ac., carb-v., chel., chin., coff., colch., conv., cupr., cur., elaps,
ferr-m., Helon., hep., iris, kali-chl., kali-n., kali-p., kreos., lac-d., lach., lac-
ac., lec., lith., Lyc., lycps., lyss., mag-s., med., mosch., morph., nat-s., nit-ac.,
op., petr., Ph-ac., Phos., pic-ac., Plb., podo., rat., sil., sulph., sul-ac., Tarent.,
Ter., thuj., Uran., zinc.26
17) Saccharine: Amy-n., arg., Ars., aur., bar-c., carb-v., chin., colo., con.,
curar., helo., kali-bi., kali-c., kali-p., kre., led., lyc., mag-c., meph., merc.,
mur-ac., Nat-m., nat-s., nit-ac., pho., PHO-AC., pic-ac., plb., ran-b., sec-c.,
sep., Sul., tarx., Thu., zin.27
18) Diabetes mellitus: (URINE-Sugar) allox,ars-br, brid-fr, cortico, cur, galeg,
helon, kali-act, lac-ac, lyc, mag-act, merc-d, morind-l, mosch, nat-m, Nat-s,
Op, pancr, phos, plb, rhus-t, sulph, syzyg, tarent, Uran-n, vinc-r.28
19) DIABETES–Sugar-Acet. Ac.; Adren.; Arg. m.; Arg. n.; Arist.; Arn.; Ars.;
Ars. i.; Aur.; Aur. m.; Bell.; bor. ac.; Bov.; Bry.; Caps.; Carb. ac.; Cham.;
Chel; Chim.; Eup. pur.; Fel.; Ferr. i.; Ferr. M.; Fl. Ac.; glon.; Glyc.; Hell.;
Helon.; Iod.; Iris; Kali act.; Kali br.; Kreos.; Lac. ac.; Lach.; Lec.; Lyc.;
Lycps. V.; Lyss.; Morph.; Mosch.; Murx.; Nat.m.; Nat. s.; Nit. Ac.; Nux v.;
Op.; Pancr.; Phase.; Ph.ac.; Phos.; Pic. Ac.; Plb.; Plb. i.; Podo.; Rhus. ar.;
sil.; Squil.; Stry. ar.; Sulph.; Syzyg.; Tarent.; Tarax.; Ter.; Uran. n.; Urea.;
Vanad.29
20) Diabetes: Ac.x., Aln., Am. Ac., Ank., Arg., (Ag.n.), Ari., Arn., As. Br.,
Asp., Bov., Calc., Ca. p., Cbl. x., Carl., cod., clch., Col., Cur., e. pu., Fe. i., Fe.
m., Fe. p., Hlon., Iod., k. ac., k.br., Kis., Lc. v., Lc. v. d., lc. x., Lrs., lcs., Mag.
s., med., Mos., Mur., na. m., Na. p., Na.s., Phas., Phlo., Ph. x., Pi.x., Plnt.,
Rat., Sac. l., Sac. o., Snc., Scil., Sec., Sil., Sti., Sul., Su. x., Syz., trx., Trl., ure.,
vic.30
6.3 AIMS AND OBJECTIVES OF THE STUDY
1. The comparative evaluation of the efficacy of both the Logico-
Utilitarian general repertories and clinical repertories.
2. Study of the clinical and general rubric from both in Logico-utilitarian
general repertories and clinical repertories in the management of type
2 diabetes mellitus.
3. To study the clinical presentation of type 2 diabetes Mellitus.
7. MATERIALS AND METHODS
7.1 PRIMARY SOURCE:
The subject for this study will be collected from OPD/IPD/ Rural camp of
Dr. B. D. Jatti Homoeopathic Medical College, Hospital and Post Graduate
Research Centre, Dharwad.
7.2 METHOD OF COLLECTION OF DATA (including sampling
procedure, if any,) Simple random sampling method.
Definition of study subject:
Subjects are considered on the basis of clinical presentations i.e., polydipsia,
polyuria, nocturia, weight loss, weakness, giddiness, blurring of vision,
muscle pain, cramps, routine investigation and urine analysis, duration of 6
weeks or more.
Following are inclusion criteria:
1) Subjects of age above 40 years and both sexes, and all ethnic groups.
2) Subjects clinically diagnosed to be having uncomplicated type 2
diabetes mellitus.
Following are Exclusion criteria:
1) Subjects with any complications of type 2 diabetes mellitus. Eg:
diabetic nephropathy, diabetic retinopathy, diabetic neuropathy etc.
2) Subjects with type 2 Diabetes Mellitus associated with any other
systemic disease.
Study sampling design:
Sampling size: Prevalence rate of diabetes mellitus in our OPD/ IPD/
peripheral OPD is 5%. Considering the 95% confidence interval at 5%
permissible error, sampling size worked out to be 76 cases. Since it is time
bound study, all admitted IPD, OPD and peripheral OPDs, cases are included
in my study period.
Study design:
The study will be a non-controlled longitudinal prospective case study.
Subjects will be selected on the basis of non-probability judgmental sampling
technique from the population of type 2 DM patients attending the OPD or
admitted to the IPD or attending peripheral OPD.
Follow up:
Patients will be seen every 15 days for 3 months and then monthly once till
the end of study period. Examination is done periodically.
Parameters used are:
Change in Clinical Findings like the Presenting Symptoms, Signs and
Investigations.
A) Controlled: Patient feels relief in the presenting symptoms either
in intensity and/ or in frequency and both fasting and post prandial
blood sugars controlled till end of the study.
B) Improved. Patient feels better of symptoms and blood sugars are
controlled but complaints reappears again and again i.e. both
fasting and post prandial blood sugar increases again and again.
C) No improvement:
i) Status quo (neither relief of symptoms nor both fasting and
post prandial blood sugars are not controlled).
ii) Drop out cases.
Study period: Nov-2010 to Nov-2012.
Statistical tests:
Appropriate test will be used depending upon the data available at the end of
the study.
7.3 DOES THE STUDY REQUIRE ANY INVESTIGATIONS OR INTERVENTIONS TO BE CONDUCTED ON PATIENTS OR OTHER HUMANS OR ANIMALS? IF SO DESCRIBE BRIEFLY.
The study requires following investigations to be conducted on patients. The study requires any following investigations to be conducted on patients.
1) FBG2) PPBG3) GLYCOSYLATED HAEMOGLOBIN4) RBS (When needed)5) URINE SUGAR IN FBG & PPBG6) URINE SUGAR IN RBS (When required)7) Routine urine and microscopic test to eliminate diabetic nephropathy 8) Eye examination (when necessary) to eliminate the diabetic
retinopathy7.4 HAS ETHICAL CLEARANCE BEEN OBTAINED FROM YOUR
INSTITUTION IN CASE OF 7.3? Yes, Ethical clearance has been obtained from the institution.
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9Signature of the candidate
10
Remarks of the guide
11 Name and Designation of (IN BLOCK LETTER)
11.1
Guide
Dr. SUDHANSU. S. MOHARANA, M.D. (Homoeo) PROFESSORPost Graduate Dept. of Repertory and Case taking, DBHP Sabah’s. Dr. B. D. Jatti Homoeopathic Medical College,Hospital & P.G. Research Center, D.C. Compound, Dharwad-580001.
11.2Signature
11.3Co-Guide (If any)
11.4Signature
11.5
Head of the Department
Dr. SUDHANSU. S. MOHARANA, M.D. (Homoeo) PROFESSOR Post Graduate Dept. of Repertory and Case taking, DBHP Sabah’s. Dr. B. D. Jatti Homoeopathic Medical College,Hospital & P.G. Research Center, D.C. Compound, Dharwad-580001.
11.6Signature
12Remarks of the Principal
12.1Signature