RAJIV GANDHI UNIVERSITY OF HEALTH SCIENCES,

BANGALORE, KARNATAKA,

ANNEXURE-II

APPLICATION FOR REGISTRATION OF SUBJECT FOR DISSERTATION

1. / NAME OF THE CANDIDATE
AND ADDRESS
(IN BLOCK LETTERS)

PERMANENT ADDRESS / DR SHEENA K N
FATHER MULLER HOMOEOPATHIC MEDICAL COLLEGE AND HOSPITAL,
UNIVERSITY ROAD, DERALAKATTE,
MANGALORE-574160,
KARNATAKA.
FLAT NO 603,
INLAND EXCELLENCY,
ARYA SAMAJ ROAD,
MANGALORE,
KARNATAKA.
2. / NAME OF THE INSTITUTION / FATHER MULLER HOMOEOPATHIC MEDICAL COLLEGE AND HOSPITAL, DERALAKATTE, MANGALORE
3. / COURSE OF THE STUDY & SUBJECT / M.D.(HOM)
ORGANON OF MEDICINE AND HOMOEOPATHIC PHILOSOPHY
4. / DATE OF ADMISSION TO THE COURSE / 16 / 6/ 08
5. / TITLE OF THE TOPIC :
“MIASMATIC EVALUATION OF HYPERLIPIDAEMIA”
6. / BRIEF RESUME OF THE INTENDED WORK
6.1 NEED FOR THE STUDY:
Raised or abnormal levels of lipids & lipoproteins in the blood has become a common clinical problem of the century which has turned out to be a challenge to the physician.
It is regarded as a highly modifiable risk factor for cardiovascular disease due to the influence of cholesterol on atherosclerosis. Hyperlipidaemia results from genetic predisposition interacting with an individual diet & lifestyle.
More than half the patients with angiographically confirmed premature coronary heart disease have a familial lipoprotein disorder which represents the most common genetic dyslipidaemia with a prevalence of 1 – 2 %.
Familial combined hyperlipidaemia characterized by elevated levels of cholesterol or triglyceride or both is estimated to cause 10 – 20 % of premature coronary heart disease & 10 % of myocardial infarction.
Secondary hyperlipidaemias constitute the vast majority of cases of hyperlipidaemia met in clinical practice. In type 2 diabetis mellitus 50% cause of death is found to be due to coronary heart disease.
Familial cholesterol hyperlipidaemia though being the most common genetic form of hyperlipidaemia, the genetic & metabolic basis of the disorder has hitherto been poorly defined.
Early detection & early control of high cholesterol in a person is an important step in reducing the development & progression of coronary heart disease & atherosclerosis. Lowering plasma cholesterol by diet & drugs slows & may even reverse the progression of atherosclerotic lesions & the complications they cause.
The expensive mode of treatment & variety of side effects in the other systems of medicine, has created an awareness in the population seeking alternative system of medicine to cure such risk factors at the earlier stage before progression into complications .Homoeopathic system of medicine is safe and based on the individual constitution and totality of expressions. The constitutional method of treatment which includes the miasmatic background of an individual has helped the sick to recover more effectively. A study in this direction is necessary to know the effectiveness of miasmatic treatment in hyperlipidaemia cases
Hence this study has been undertaken to define the existence of a relation if any with fundamental & dominant miasm in hyperlipidaemia, so that the evaluation of miasm in an individual can help in early detection of predisposition for hyperlipidaemia & thus help in the prevention.
6.2 REVIEW OF LITERATURE
Plasma levels of cholesterol & triglyceride beyond 95th percentile for age & sex is termed hyperlipidaemia.
Lipid is an essential chemical in the body. Besides their role in cellular structure, hormones & various other biochemical function, most of the triglycerides are stored in adipose tissue. They are the highly concentrated form of energy which can support body’s energy needs for long periods of food deprivation.
Insoluble lipids are solubilized in association with protein as lipoprotein & transported. Chylomicron, Very low density lipoprotein (VLDL), Low density lipoprotein (LDL), High density lipoprotein (HDL) & albumin free fatty acids are different lipoprotein complexes that transport lipid in blood.
50 % is excreted through bile & 50 % is converted to bile acids which are excreted as bile salts.
LDL is more atherogenic while VLDL are less atherogenic. HDL helps in removing cholesterol & hence non atherogenic.
1% increase in coronary heart disease risk for each 1% increase in LDL cholesterol & 2 – 3% reduction in coronary heart disease risk for each 1% increase in HDL cholesterol is generally seen
Any defect in the synthesis, transport or excretion of the lipids cause a rise in their level in plasma which becomes a risk factor for coronary heart disease which is one of the major cause of death.
Etiology
Primary causes of hyperlipidaemia
·  Decreased clearance of LDL
·  Excess triglyceride & apoprotein production
·  Overproduction of VLDL
·  Clearance defect of triglycerides
Secondary causes of hyperlipidaemia
·  Hypothyroidism
·  Nephrotic syndrome
·  Chronic liver disease
·  Anorexia nervosa
·  Stress
·  Glycogen storage disease
·  Diabetis mellitus
·  Pancreatitis
·  Obesity
·  Sepsis
·  Malnutrition
·  Malabsorption
·  Myeloproliferative diseases
·  Chronic infectious diseases
·  Hyperthyroidism
·  Excess alcohol consumption
·  Diet rich in saturated fat
·  Drugs like oral contraceptives
·  Cigarette smoking
Classification
·  Primary hyprlipidemia - An inherent genetic defect of lipid metabolism
1.  Familial combined hyperlipidemia
2.  Familial hypertriglyceridemia
3.  Familial hypercholesterolemia
4.  Polygenic hypercholesterolemia
5.  Familial type III hyperlipoproteinemia
6.  Familial lipoprotein lipase deficiency
7.  Familial C II apoprotein deficiency
·  Secondary hyperlipidemia - Secondary to other diseases.
Clinical features
·  Xanthoma
·  Xanthelesma
·  Arcus cornea
·  Atherosclerosis
Diagnosis
Lipid profile – Triglycerides > 150 mg/dl
Cholesterol > 200 mg/dl
HDL < 40 mg/dl
LDL > 130 mg/dl
Complications
·  Coronary heart disease
·  Cerebral vascular disease
·  Peripheral vascular disease
Hahnemann’s pathology is based on dynamical theory of disease i.e. Disease is primarily a morbid dynamic functional disturbance of vital principle
“Useful to the physician in assisting him to cure are the particulars of the most probable exciting cause of acute disease, to enable him to discover its fundamental cause, which is generally due to chronic miasm. In these investigations, the ascertainable physical constitution of the patient (especially when the disease is chronic), his moral & intellectual character, his occupation, his age, sexual function etc, are to be taken into consideration” – Aphorism 5.
To Hahnemann it gradually became clear that such chronic conditions cannot be cured by the vital force alone, nor by any manipulation of diet or life habits. He then launched into exhaustive inquiries of all such chronic cases to see if any common denominator could be found to explain the deep & invisible weakness which predisposed to their chronic condition – A weakness which Hahnemann termed miasm. These weakness were transmitted from one generation to next according to Hahnemann’s investigations which included whenever possible, interviews with the ancestors of chronic disease patients
Children inherit from each parent particular sensitivities in particular organs & the resulting disorder in the child is either an accurate copy of one parent’s disorder or a compounding of disorders inherited from both the parents - George Vithoulkas.
The diseases are built accordingly on four different plans – Occupational / drug disease, Psora, sycosis & syphilis.
In all human beings we will find a portion of all three pathological characteristics. Yet one will always be dominant, preponderant, modulating & determining more strongly the biological structures as well as those of soul &character – Dominant miasm.
Characteristic guiding symptoms from present condition of patient is linked with earlier development depicted in past history & family history – Fundamental miasm
The reality of miasm in a patient is always expressed by signs & symptoms the patient produces which permit the individual expression of characteristics of miasm which allow to determine, recognize & wholly handle the patient individuality – ICR manual Area C.
Miasmatic trump cards are the best to prove supremacy of homoeopathy among other methods of treatment in chronic & incurable illness with a stamp of unknown cause(s). For better generation we have to study chronic miasms & treat the people homoeopathically. We can study miasmatic medicines to improve future generation through a long course of treatment
With homoeopathic knowledge & understanding miasmatic disease we can improve mentally & physically near & dear relatives
.
Find the chronic miasms, treat them well & let us live in peace & harmony – Ramanlal. P.Patel.
.
6.3 OBJECTIVES OF THE STUDY
1.  To assess the role of miasm in hyperlipidaemia.
2.  To study the different types of hyperlipidaemia.
7. / MATERIALS AND METHODS
7.1. SOURCE OF DATA
The subjects of the study will be selected from the patients with hyperlipidemia attending OPD, IPD and peripheral centres of Fr Muller Homoeopathic medical college hospital as per inclusion criteria.
7.2 METHODS OF COLLECTION OF DATA
The Materials used for the Study:
A minimum of 30 cases would be selected. All these cases would be represented in the standardized case record & analyzed for serum lipids. According to the guidelines given in SCR, case would be analyzed, processed & the miasm erected.
Inclusion Criteria:
·  All cases with hyperlipidemia between the age group 40 yrs and 75yrs, from both sexes would be selected.
·  Subjects who have diagnosed of hyperlipidemia based on clinical history, clinical presentation, clinical examination and blood investigation.
Exclusion Criteria:
·  Subjects below 25 years and above 75 years
·  Subjects with serious complications like Myocardial infarction, Stroke etc.
Method of analysis:
With reference to the objective, among the thirty samples, the miasms in hyperlipidaemia will be analysed in terms of ratios
7.3 Does the study require any interventions to be conducted on patients, or other humans (or animals)? If so please describe briefly.
Yes, Lipid profile of the subject is required in this study
7.4 Has ethical clearance been obtained from your institution in case of 7.3?
Yes, enclosed.
8. / LIST OF REFERENCES
1.  Sthyanarayana. U, Chakrapani. U . Biochemistry. 3rd ed. Kolkata : Books & Allied (P) Ltd; 2006. p 285 – 287
2.  Vasudevan. D.M, Sreekumari. Text book of biochemistry. 5th ed. New Delhi: Jaypee brothers, Medical publishers (P) Ltd;2007. p 148 – 163
3.  Mcphee J. Stephen, Papadakis A. Maxine,Tierney M. Lawrence. 2008 Current Medical Diagnosis and Treatment. 47th ed. USA: Mc Graw Hill; 2008. p1074 – 1076
4.  Shah N Siddharth. API Text book of Medicine.7th ed. Mumbai: The Association of physician of India; 2006. p 250 – 257
5.  Braunwald, Fauci, Kasper, Hauser, Longo, Jameson. Harrison’s principles of internal medicine Vol II. 15th ed.USA: Mc Graw Hill; 2001. p 2250
6.  Hahnemann Samuel. Organon of medicine. 6th ed. New Delhi: B Jain publishers Pvt Ltd; p 94.
7.  Vithoulkas George. Homoeopathy medicine for the new millennium.26th ed New york: Arco publishing;2000. p 32,36
8.  Dhawale. M.L. Principles and practice of homoeopathy, 3rd ed. Bombay : Institute of clinical research; 2000.p28
9.  Dhawale.M.L. Hahnemanian totality symposium Part II Area c.2nd ed. Mumbai: Institute of clinical research; 2000.pc-16,c-19
10.  Patel P. Ramanlal. Chronic miasm in homoeopathy and their cure with classification of their rubric/symptoms in Dr.Kent’s repertory, Kottayam: Hahnemann book house;1996. p6, 7,75.
11.  www.pubmed.org – hyperlipidemia, September 2008
12.  www.wikepedia.com – hyperlipidemia, September 2008
9. / SIGNATURE OF THE CANDIDATE.
10. / REMARKS OF THE GUIDE.
11. / 11.1. NAME AND DESIGNATION OF GUIDE
(In block letters). / DR. ROSHAN PINTO, BHMS ,MD (HOM),
DEPT. OF ORGANON OF MEDICINE AND HOMOEOPATHIC PHILOSOPHY,
FR. MULLER HOMOEOPATHIC MEDICAL COLLEGE, DERALAKATTE, MANGALORE
11.2. SIGNATURE.
11.3. CO-GUIDE.
11.4. SIGNATURE.
11.5. HEAD OF THE DEPARTMENT. / DR. SHIVAPRASAD K, B.Sc, BHMS MD (HOM), PROFESSOR & HOD,
DEPT. OF ORGANON OF MEDICINE AND HOMOEOPATHIC PHILOSOPHY,
FR. MULLER HOMOEOPATHIC MEDICAL COLLEGE, DERALAKATTE, MANGALORE
11.6. SIGNATURE.
12. / 12.1. REMARKS OF THE
CHAIRMAN & PRINCIPAL.
12.2. SIGNATURE.