From:

Dr. MINU. P.

Post Graduate Student,

Post Graduate Dept. of Repertory and Casetaking,

DBHP Sabah’s. Dr. B. D. Jatti Homoeopathic MedicalCollege,

Hospital & P.G.ResearchCenter,

D.C. Compound, Dharwad-580001.

To:

The Registrar

RajivGandhiUniversity of Health Sciences, Karnataka,

Bangalore.

Through:

The Principal

DBHP Sabha’s. Dr. B. D. Jatti Homoeopathic MedicalCollege,

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 THEMANAGEMENT OF TYPE 2 DIABETES MELLITUS”

I am herewith enclosing completed proforma of synopsis for registration of subject for dissertation.

Thanking you,

Place: DharwadYours 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

RAJIVGANDHIUNIVERSITY OF HEALTH SCIENCES KARNATAKA, BANGALORE,

BY

Dr. MINU. P

Through

DPHP’s

DR. B. D. JATTI HOMOEOPATHIC MEDICALCOLLEGE, 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 MEDICALCOLLEGE, HOSPITAL & P.G. RESEARCH CENTER, D.C. COMPOUND, DHARWAD-580001.

(KARNATAKA)

RAJIVGANDHIUNIVERSITY 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 MedicalCollege, Hospital & P.G.ResearchCenter,
Dharwad-580001
PERMANENT ADDRESS / Dr. MINU. P.
D/o. P. Gangadharan
58/1, “Sree Ganga”
J.R. Colony,
New Thippasandra
BANGALORE-560075
2. / NAME OF THE INSTITUTION / D.B.H.P. Sabha’s
Dr. B. D. Jatti Homoeopathic MedicalCollege, Hospital & P.G.ResearchCenter,
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 oneof 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 inBritain 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 outerageousevidence 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’scharacteristics 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 comparativeefficacy of logico-utilitarian repertories andclinical 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.1Diabetes 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
  1. 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
  2. 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.
  1. 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
  1. The prevalence diabetes mellitus in India is currently reported around 13-15%.7The 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
  1. Type 2 diabetic mellitus is principally a disease of the middle aged and elderly usually above the aged of 40 years.11
  1. 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 underactivity. 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
  1. 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
  1. 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.19The late complications are Diabetic retinopathy, Diabetic nephropathy, Diabetic neuropathy, Cardiovascular diseases,20Diabetic 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.