presentation on malaria 2007

Views:
 
     
 

Presentation Description

No description available.

Comments

By: asifshahms (30 month(s) ago)

allow to download.

By: civilsurgeon (37 month(s) ago)

nice ppt

By: deepamalliga (38 month(s) ago)

hai this presentation wonderful and very informative ..............can u share for me

By: agcooldoc (43 month(s) ago)

nice presentation kindly post me this presentation

By: maisara (46 month(s) ago)

yup!superb ppt..can i download?tq

See all

Presentation Transcript

Slide 1: 

MALARIA DR .RONISH JOS CHALAKKAL . BAMS. MD. (AY)

MALARIA : 

MALARIA DEFENITION Malaria is a febrile illness caused by a hemo protozoa of the genus Plasmodium. CHARACTERS periodic Fever Splenomegaly Hemolytic Anaemia TYPES P.Ovale _ Ovale tertian P. Malaria _ Quartan malaria P. Vivax _ Benign tertian P. Falciparum _ Malignant malaria

Endemicity Of Malaria : 

Endemicity Of Malaria Factors determining are, (1) Presence of susceptible population. (2) High population of vector mosquitoes. (3) Presence of vector mosquitoes. Reservoir host, (1) Chimpanzee _ In Africa (2) Migrating Birds _ Other parts of world.

Epidemology : 

Epidemology Endemic to all tropical countries. India, Bangladesh, Srilanka, Africa etc. Rare in altitudes above 2000 m. Rare in places of low temperature. One of 3 diseases causing maximum mortality. Ie, Tuberculosis, Measels $ Malaria. Occurs in about 100 countries.

India : 

India The annual incidence in 1976 – 7 Million. 6 million P. Vivax & 1 million P. Falciparum cases. In 2003 ,1.64 million cases & 943 deaths. Maximum cases & deaths in Orrisa. 4 deaths were reported in Kerala. P. Falciparum – Tripura, Meghalaya, Orrisa, Nagaland, Bihar, Assam & Manipur. P. Malariae – Reported only in Karnataka. P. Vivax – Other parts of India.

Deaths/indian states : 

Deaths/indian states

WORLD scenario : 

WORLD scenario 500 million cases annually with 2.7 million deaths. Almost half of the African countries are at risk. Mortality rate is 1.1 – 2.7 million/ year. 25% of child mortality in Africa.

MILESTONES OF RESEARCH ON MALARIA : 

MILESTONES OF RESEARCH ON MALARIA 1716 – Lancisi - Connection b/w mosquito and malaria. 1880 _ Laveran - Discovered Plasmodium in human blood. 1885 _ Golgi - Erythrocytic Schizogony in man. 1891 _ Ramnowsky - staining of blood film. 1894 _ Manson - Role of mosquito in malaria. 1897 _ Ronald Ross - Sexual cycle in mosquito. 1936 _ Paul Muller - DDT invention. 1948 _ Short& Graham - Pre erythrocytic schizogony. 1969 _ Rudzinska - Fine structure of plasmodium.

PLASMODIUM _ SYSTEMIC POSITION : 

PLASMODIUM _ SYSTEMIC POSITION Phylum _ Protozoa Sub phylum _ Sporozoa Class _ Telesporea Sub class _ Coccidia Order _ Eu Coccidia Sub order _ Haemosporina Genus _ Plasmodium Species _ About 60 known species.

sporozoite : 

sporozoite

VECTOR : 

VECTOR Vectors are female Anophelene mosquito. Types in India are : A. Culcifacies A. Stephensi A. Fluviatilis A. Minimus A. Dirus A.Sundaicus

DIFFERENTIATING ANOPHELES & CULEX : 

DIFFERENTIATING ANOPHELES & CULEX ANOPHELES Adult Slender body Legs with hairs Body inclination 45 degree Spotted wings Cannot fly long Larvae Surface feeder Dark colour & small No respiratory siphon 45 degree angle to water surface CULEX Adult Stout body Legs without hairs Parralel at rest Wings uniform colour Can fly long Larvae Bottom feeder Light colour & larger Siphon present Parallel to water surface.

DIFFERENTIATING ANOPHELES & CULEX : 

DIFFERENTIATING ANOPHELES & CULEX EGGS In fresh & clean & clean water Seen singly Boat shaped Have air floats. EGGS In dirty water Seen as a cluster Cigar shaped No air floats.

DIFFERENTIATING ANOPHELES & CULEX : 

DIFFERENTIATING ANOPHELES & CULEX

PREVALANCE OF MALARIA : 

PREVALANCE OF MALARIA 1. Spleen Rate : Represents the % of children in age group of 2-9 yrs showing palpable spleens.- 2. Parasite Rate : Represents the % of +ve cases of malaria detected by the examination of blood film in a community. 3.Infant Parasite Rate : Represents the % of +ve cases among Children aged 0 – 11 months.

CLASSIFICATION OF ENDEMICITY : 

CLASSIFICATION OF ENDEMICITY

HOST FACTORS : 

HOST FACTORS AGE - All ages are affected New borns considerably resistant. SEX- Males more exposed to outdoor. Better clothing of females. RACE- Sickle cell hemoglobin more resistant. PREGNANCY- Primigravids at more risk. HOUSING- Ill ventilated & ill lighted house harbours more mosquitoes. POPULATION MOBILITY- Migration,emigration

HOST FACTORS : 

HOST FACTORS OCCUPATION-mainly rural disease, related to agriculture practice. HABITS-outdoor sleep, nomadic habit. IMMUNITY- Infants born of immune mothers protected during first 3-5 months by maternal IgG antibodies. ECONOMY – Developed socio economic areas having low intensity.

COURSE AND PROGNOSIS : 

COURSE AND PROGNOSIS Course of all forms of malaria is chronic. Primary attack subsides to relapse again even without treatment. Each relapse may last for several weeks. Spleen enlarges sucessievely with each relapse. Anaemia and Jaundice develops. Patient gradually becomes home bound. Nutritional adequacy develops. Working capacity declines. This is the stage of chronic malaria.

CURRENT INCIDENT LEVEL MEASUREMENT : 

CURRENT INCIDENT LEVEL MEASUREMENT Annual Parasite incidence (APT) = Confirmed cases during 1 yr x 1000 Population under surveillance Annual blood examination rate (ABER) = Number of slides examined x 100 Population Annual Falciparum incidence (AFI). Slide possitivity rate (SPR).

IN CASE OF FEVER ,MALARIA SHOULD BE SUSPECTED IN : 

IN CASE OF FEVER ,MALARIA SHOULD BE SUSPECTED IN An un explained fever Pregnant woman After child birth in post partum period Post operative period Mal nutrition In association with acute or chronic infections Blood transfusion

DIAGNOSIS : 

DIAGNOSIS Suspicion strengthen in presence of Jaundice, Splenomegaly, Anaemia. Recent visit to endemic areas strngthen diagnosis. Using Ramnowsky stained films. Thick films – for searching the parasite. Thin films – for identifying the species. If Plasmodium present in erythrocytes - - Chromatin will be red. - Cytoplasm will be blue.

DIFFERENTIAL DIAGNOSIS : 

DIFFERENTIAL DIAGNOSIS Sinusitis Urinary tract infection Infective endocarditis Hepatic amoebiasis Septicemias Relapsing fever Tuberculosis Hepatosplenomegaly in chronic malaria. Has to be distinguished from: Portal hypertension Hemolytic anaemia Lymphomas

LAB DIAGNOSIS : 

LAB DIAGNOSIS Fluorochrome staining Quantitative buff coat analysis (QBC) Fluorescence activated cell sorter (FACS) Anti malarial Antibody detection. Antigen detection test by ELISA. Dip Stick Assay Antigen Capture.

PRECAUTIONS FOR LAB INVESTIGATIONS : 

PRECAUTIONS FOR LAB INVESTIGATIONS 0.5 ml adrenaline inj subcutaneously 15 mts prior to blood examination, increases +ve rate Supressive drugs should be stopped for 2 days prior to blood examination. Bone marrow blood may have to be examined for fine diagnosis

INCUBATION PERIOD : 

INCUBATION PERIOD Falciparum _ 12 (9 - 14) days. Vivax _ 14 (8 -17) days. Quartan malaria _ 28 (18 – 40) days. Ovale _ 17 (16 -18) days.

C/F OF VIVAX MALARIA : 

C/F OF VIVAX MALARIA I P _ 10 -15 days. Fever, headache, discomfort, nausea, vomiting. After 2 weeks only, periodicity of fever seen. Paroxysms occur in 3 stages - (1) Cold stage (2) Hot stage (3) Sweating stage. COLD STAGE - Starts with chills & rigor. - Temp shoots upto 40 degree celsius or more & rapid pulse. - Skin becomes pale & cold.

Slide 28: 

HOT STAGE - The hot stage sets in 30 - 60 min. - Flushing of skin. - Bounding of pulse. - Severe headache. - Restlessness. - Hyper pyrexia in non immunes. - Herpes labialis is common.

Slide 29: 

SWEATING STAGE - Sweating starts after 2 – 6 hrs. - Temp rapidly comes down to normal. - Pulse becomes slow. - Patient goes to sleep, fully exhausted & dehydrated, to wake up fresh.

FEVER CYCLE IN VIVAX MALARIA : 

FEVER CYCLE IN VIVAX MALARIA

c/f vivax malaria : 

c/f vivax malaria These paroxysms repeat at each 48 hrs Temp is normal between attacks Paroxysms recur for about 3 months Then subsides even with out treatment Late relapses may occour even after 2-3 yrs By 2wks of illness liver & spleen palpable. Vivax malaria not usually fatal

C/F OF FALCIPARUM MALARIA : 

C/F OF FALCIPARUM MALARIA IP – 10 -14 days. Bodyache, headache, vomiting more severe than vivax malaria Disease starts acutely or classical 3 stages or atypically. Patient not well in between febrile paroxysms. Periodicity either daily or less than 48 hrs. Fatal complication at any time.

C/F OF FALCIPARUM MALARIA : 

C/F OF FALCIPARUM MALARIA In mixed infections p.falciparum predominates Rapid haemolysis & anaemia Haemoglobinuria in severe cases Neutropenia is common Pregnancy may cause abortion or premature delivery

SEVERE FALCIPARUM MALARIA AS PER WHO : 

SEVERE FALCIPARUM MALARIA AS PER WHO 1. cerebral malaria 2.severe anaemia 3.renal failure. 4. pulmonory oedema. 5. hypoglycemia. 6. low systolic b.p 7. spontaneous haemmorage. 8.repeted generalised seizures. 9. acidosis 10. haemoglobinuria

C/F of PLASMODIUM MALARIA : 

C/F of PLASMODIUM MALARIA IP _ 1 to several month. Fever occurs with quartan periodicity. Rigor may be absent at onset. Hepato splenomegaly is common. Antigen – Antibody complex causes Nephrotic syndrome. Peripheral blood shows all stages of parasite.

CLINICAL FEATURES OF OVALE TERTIAN : 

CLINICAL FEATURES OF OVALE TERTIAN Very similar to vivax malaria But mild paroxysms may be milder

RELAPSES IN MALARIA : 

RELAPSES IN MALARIA Even if further infection is avoided, relapses may occur For 1 _ 3 yrs in case of P. vivax. Upto 1 year in case of P. ovale. Upto 1 year in case of P. falciparum. Several years (even 20) in case of P. malaria.

IMMUNITY AGAINST MALARIA : 

IMMUNITY AGAINST MALARIA In hyper & holo Endemic Areas – locals immunity – due to the repeated encounter with the parasite. Though parasite in blood – no clinical symptoms. This phenomenon is premunity. Children and infants suffer heavily. In hypo & meso endemic areas, local inhabitants do not acquire strong immunity. Single attacks do not give immunity because parasite undergoes rapid antigenic variations especially P. falciparum.

Immunity against malaria cont… : 

Immunity against malaria cont… Repeated attacks produce immunity Abnormal rbc inhibit devolepment of parasite Rbc having G-6 pd deficiency inhibits it Sickle cell haemoglobin inhibits parasite Alpha & beta thalessimias have partial protection _ve blood group show resistance, especially for vivax

ANTIMALARIAL DRUGS : 

ANTIMALARIAL DRUGS Chloroquine Quinine Proguanil Pyrimethamine Sulphadoxin Mefloquine Cortimoxazole Tetracycline Artemesinin Primaquine

MALARIAL VACCINE : 

MALARIAL VACCINE Asexual blood stage vaccine _ Based on antigens derived from the blood stages of P. falciparum. SPF 66 Vaccine – from USA Trials now going on African countries.

ENVIRONMENTAL FACTORS : 

ENVIRONMENTAL FACTORS Season : max from june – nov in India. Temperature : 20 – 30 degree celsius, ideal for parasite. temp lower than 16 degree celsius ] lethal to temp higher than 30 degree celsius ] parasite. Humidity : Relative humidity 60% ideal for mosquitoes. When humidity high, mosquito more active. When humidity low, mosquito do not live long. Rainfall : Increses breeding place Altitude : No anophelus above 2500 mts. Manmade factors : Garden pools,irrigation channels, etc

MOSQUITO CONTROL : 

MOSQUITO CONTROL Elimination of breeding places Destruction of larvae and pupae Destruction of adult mosquitos Defence against mosquito bite

ELIMINATION OF BREEDING PLACE : 

ELIMINATION OF BREEDING PLACE Drain out swampy areas and stagnant water Domestic water holding utilenses be kept closed Filling up of mosquito breeding grounds Bushes and shrubs shuld be cleared

DESTRUCTION OF LARVAE AND PUPAE : 

DESTRUCTION OF LARVAE AND PUPAE Spray open water bodies with oil or kerosine. Emulsions of DDT and BHC. Paris green powder. Larvicide fishes. Natural enemies like dragonfly,aquatic insects. Tulsi seeds . Extract of aquatic weed ceratophyllum demersum

DESTRUCTION OF ADULT MOSQUITOES : 

DESTRUCTION OF ADULT MOSQUITOES Drive out or kill by fumigation Pyrethrum,sulpher for fumigation Smoke of garlic Residual spray of DDT effect for months Mosquito traps Sterilisation by genetic engineering Pheromone traps

FACTS : 

FACTS Chloroquine resistant strains of P. falciparum in north eastern states of India. Mixed infectious increasingly seen. Usual combination is P. falciparum & P. vivax. In combination symptoms of P. falciparum predominates.

AIRPORT MALARIA : 

AIRPORT MALARIA Occurance of malarial incidents near airports. Due to exotic infective mosquitoes. This is termed as Commuted Malaria. Eg: in TVM airport in 1995 – 96.

COMPLICATIONS OF MALARIA : 

COMPLICATIONS OF MALARIA Complications arise mainly due to P. falciparum. Chance of complication is more when more than 5% RBC is parasitised. Complications include Cerebral malaria Malarial hyperpyrexia Gastro intestinal complications Hepatic complications Renal failure Algid malaria Black water fever.

CERBRAL MALARIA : 

CERBRAL MALARIA Occlusion of micro circulation of brain. Sludging of parasitised erythrocytes. Arterial damage occurs. Pathology Sequestration of infected erythrocytes Micro vasculature is blocked Release of neurotoxic cytokinins

SYMPTOMS : 

SYMPTOMS Hyper pyrexia Head ache Convulsions Coma Paralysis Neuro psychateric disturbances. High tension of C.S.F.

Slide 52: 

Symptoms resembles acute inflammatory disorders of brain. Differentiated from meningitis as in cerebral malaria. Pleocytosis is not prominent. Fatal if left untreated. In early stages drugs are effective. Bad prognosis in advanced condition. Mortality rate 10-30% even in well equiped centres.

NEUROLOGICAL COMPLICATIONS : 

NEUROLOGICAL COMPLICATIONS Develops in 10% of cases. Hemiplegia, paraplegia, cranial nerve palsies, cerebellar dysfunction & psychosis. Post malarial complication may develop even after full clinical recovery & parasite clearance. Includes convulsions, cerebellar ataxia, tremor, psychosis.

ALGID MALARIA : 

ALGID MALARIA Occurs in patients with gastro intestinal manifestations. Extreme dehydration & shock without warning signs. Surface temp drops, rectal temp elavates. Manage as in emergency. If not mortality very high.

GASTRO INTESTINAL COMPLICATIONS : 

GASTRO INTESTINAL COMPLICATIONS Nausea, vomiting, epigastric tenderness, haemetemisis & diarrhoea. Stools watery as in cholera. Stools blood stained as in dysentry. Jaundice, hepatomegaly. Acute renal failure may develop, hence mortality rate at 30%.

BLACK WATER FEVER : 

BLACK WATER FEVER Rare complications. Occurs in patients of chronic falciparum malaria. Immune mechanism here acts as –ve factor as it destroys both parasitised & non parasitised RBC. Sudden intra vascular haemolysis & it causes fever, rigor, anaemia & haemoglobinuria.

METABOLIC COMPLICATIONS : 

METABOLIC COMPLICATIONS Hypoglycemia – due to depletion of liver glycogen. Impairment in gluconeogenesis. Young children & pregnant women most affected.

MALARIA IN PREGNANCY : 

MALARIA IN PREGNANCY Maternal death, abortion, still birth, premature delivery, low birth weight babies. Hypo glycemia, pulmonary oedema more frequent. Placenta is the site of malarial parasite. Congenital malaria in new born is rare.

ANAEMIA : 

ANAEMIA Most common complication of malaria. Destruction of parasitised erythrocytes leads to nutritional deficiencies of Folate, Iron, vit B12 &Proteins. Rapid fall of Hb below 7g/dl may necessitate blood transfusion.

IDIOPATHIC PULMONARY OEDEMA : 

IDIOPATHIC PULMONARY OEDEMA Mortality of 50% Occours in persons showing apparent response to specific treatment.

NATIONAL ANTI MALARIA PROGRAMME : 

NATIONAL ANTI MALARIA PROGRAMME NATIONAL MALARIA CONTROL PROGRAMME—1953 -residual DDT spraying where spleen rate over 10% -operated for 5 yrs (1953– 58) 75 million cases in 1953 reduced to 2 million cases in 1958 -nearly 80% reduction NATIONAL MALARIA ERADICATION PROGRAMME --- 1958 - almost failure - cases increased from 50000 in 1961 to 6.4 million in 1976

Slide 62: 

-MODIFIED PLAN OF OPERATION 1977 -NMEP renamed as NATIONAL ANTI MALARIA PROGRAMME in 1999 -ENHANCED MALARIA CONTROL PROJECT sponsored by world bank in1997 -ROLL BACK MALARIA by WHO in 1998

TREATMENT : 

TREATMENT Includes 3 stages --SUPRESSIVE THERAPY --PREVENTION OF RELAPSE --TREATMENT FOR COMPLICATIONS

DISTRIBUTION OF PARASITE : 

DISTRIBUTION OF PARASITE P.VIVAX 70% IN INDIA P.FALCIPARUM 25—30% IN INDIA P.MALARIAE 1% IN INDIA P.OVALE CONFINED TO TROPICAL AFRICA &VIETNAM

LIFE CYCLE OF PARASITE : 

LIFE CYCLE OF PARASITE 2 STAGES ---- SEXUAL CYCLE – IN MOSQUITO- SPOROGONY ASEXUAL CYCLE – INMAN- SCHIZOGONY

LIFE CYCLE OF MALARIA PARASITE : 

LIFE CYCLE OF MALARIA PARASITE

STRUCTURE OF A TROPOZOITE : 

STRUCTURE OF A TROPOZOITE

ASEXUAL CYCLE – SCHIZOGONY : 

ASEXUAL CYCLE – SCHIZOGONY Pre erythrocytic phase in liver Multiply by schizogony Cryptozoocytes Metacryptozoocytes---attack rbc Trophozoite Signetorystage (vacule) SchizogonySchizont Neuclear division , multiple fission Merozooites ---(comes out of rbc) Gametozytes Slightly enlarge (macrogametocytes) Throw away cytoplasm & becomes compact (microgametocytes) Leave human as gametocytes

SEXUAL CYCLE –SPOROGONY –IN MOSQUITO : 

SEXUAL CYCLE –SPOROGONY –IN MOSQUITO MACROGAMETOCYTE-round up to-MACROGAMETE MICROGAMETOCYTE-round up to-MICROGAMETE Exflagellation Microgamates encircle macro gametes Fertilization occours—so now diploid stage Ookinite Oocyst Multiple fission(sporogony) Sporocytes(haploid) Migration to salivary glands Now mosquito is ready for infection

̭̘ͥÌ`¥Ìœú˜ÌÆ : 

̭̘ͥÌ`¥Ìœú˜ÌÆ . zùÌâ­ÌÌâ +ŸÌÌâ +Í·þt̲ÌÉ—ÌÜtÌÌâ `¥ÌœúÌât²Ìß®õ²™Ì ¥ÌÌ ÌٍÌ:* ŒÌÌtÌ٘̍™Ìt̘ÌÉ Ìë̏™Ì FòœúÌâÍtÌ Í¥Ì­Ì˜Ì`¥Ìœú˜ÌÆ ** (M.N.) . Fßò¨Ì̍ÌÌÉ ¥™ÌÌÍQ̘ÌÙHò̍ÌÌÉ Í˜Ìy™ÌÌ·þÌœúÌÍzù²Ìâͥ̍ÌÌÉ* +ŸÌÌâ +ÍÌ zùÌâ­ÌÌâ zÜù­™Ì̆æœÆú ¡ô–Q¥ÌÌ +™Ìt̘ÌÌâ –Ì¡ô˜ÌÆ** ²Ìͥ̏ÌKÌÌâ `¥Ìœú˜ÌÆ FÙò™ÌÌÊtÌÆ Í¥Ì­Ì˜ÌÉ K̙̥ÌßÍ}ù—ÌÌFÆò* (A.H.Ni) *

Slide 71: 

As per Madhavacharya, FâòÍZÌtÌÆ —ÌÜtÌÌÍ—Ì­ÌÉOÌÌâHÉò –ÌêÜ¥ÌtÌâ ̭ͥÌ`Ìœú˜ÌÆ* . Ìę̙̈Ì: ²Ì͍̏ÌÌtÌâÌ zÙù®õÌ ÌfÌÍ¥ÌQÌÌ `¥ÌœúÌ* ²Ì͍̏ÌÌtÌâ tÌÙ ™ÌÌâ —ÌÜ™ÌÌtÌÆ ²Ì: zùÌâ­Ì: ÌÍœúFòÕÏtÌtÌ:* (c.s.ch.chi)

tÌßtÌÕ™ÌFò `¥Ìœú˜ÌÆ : 

tÌßtÌÕ™ÌFò `¥Ìœú˜ÌÆ . ....˜ÌâzùÌâÌÌÍ¡ô²tÌßtÌÕ™ÌFâò* OÌëÌÍ·þ ͏ÌuÌÌ̡͍ôÌtÌÆ ˜ÌÜ}ùύÌ: ÍwÌFò²™Ì Fò•ò͏ÌuÌtÌ:** . ²Ì Ìß®õ²™ÌÌ̡͍ôFò•òÌtÌÆ ²Ì ZÌæFòÌ·þ̍tÌœú: ²˜ÌßtÌ:** (A.H.Ni) . tÌßtÌÕ™ÌFò: tÌßtÌÕ™Ìâ +͹þ* (M.N)

ZÌtÌÙtyÌÊFò `¥Ìœú˜ÌÆ : 

ZÌtÌÙtyÌÊFò `¥Ìœú˜ÌÆ . ²ÌÉͬÌtÌ: ˜Ìâzù²ÌÌâ ˜ÌÌOÌË zùÌâ­Ì©ÌÌÍÌ ZÌtÌÙtyÌÊFÉò* ÍzùÌˆù™Ì˜ÌÆ ™ÌÌâ ̬̘ͥ™Ì Ìët™ÌâÍtÌ ²Ì ZÌtÌÙtyÌÊFò:**(C.S.Chi) . ZÌtÌÙtyÌä +͹þ ZÌtÌÙtyÌÊFò:*(M.N.)

TREATMENT : 

TREATMENT Fò˜ÌʲÌÌQÌÌœúsÌÉ `Ì»ÌtÌÆ tÌßtÌÕ™ÌFòZÌtÌÙtyÌÊFòÌæ* +ÌO̍tÌÙœúÌٖ̍QÌÌâ Í·þ Ìę̙̈ÌÌâ ̭̘ͥÌ`¥Ìœú˜ÌÆ** (C.S.Chi) Daivavyapashraya chikitsa Yuktivyapashraya chikitsa

DAIVAVYAPASHRAYA CHIKITSA : 

DAIVAVYAPASHRAYA CHIKITSA ˜ÌsÌՍÌ̘ÌÌâ­ÌŒÌՍÌÌfÌ ˜ÌÉOÌŸ™Ì̍ÌÌÉ Í¥Ì­Ì²™Ì ZÌ* ŒÌÌœúsÌÌzùOÌzù̍ÌÌfÌ ²Ìâ¥ÌÌÌtÌÆ Ì —Ì¥Ìâa¥Ìœú:** —ÌHòšÌ ˜ÌÌtÌÙ: ͏ÌtÌß©ÌæÌÉ OÌÙœÆú>ðsÌÌÉ ÌÜ`̍ÌâÌ ZÌ* –ÌêºZÌ™ÌäsÌ t̲̏ÌÌ ²Ìt™ÌâÌ ͍̙̘ÌâÌ ZÌ** `̷̏þÌâ˜ÌÌëŒÌ̍ÌâÌ ¥Ìâzù̍ÌÌÉ ¬Ì¥ÌsÌâÌ ZÌ* `¥ÌœúÌtÌÆ Í¥Ì˜ÌÙZ™ÌtÌâ ¨ÌÕQÌìÉ ²ÌÌŒÌ܍ÌÌÉ zù¨ÌʍÌâÌ ZÌ** (C.S.Chi)

Yuktivyapashraya chikitsa : 

Yuktivyapashraya chikitsa Vata -¥ÌÌt̏ÌëŒÌ̍ÌÉ ²ÌϏÌÍ—Ì: ¥ÌѲtÌÍ—Ì: ²Ì̍ÌÙ¥Ì̲̍Ìæ:* Í´ÌOŒÌÌâ­sÌæœúÌÌ̍Ìæ©Ì ˜Ì™ÌâtÌÆ Í¥Ì­Ì˜Ì`¥Ìœú˜ÌÆ** Pitta-̜ͥâúZ̍ÌâÌ Ì™Ì²ÌÌ ²ÌϏ̭ÌÌ ²ÌɲFßòtÌâÌ ZÌ* ̭̘ͥÌÉ ÍtÌHò¨ÌÕtÌæ©Ì `¥ÌœÉú ͏ÌuÌÌâuÌœÉú `Ì™ÌâtÌÆ** Kapha -¥Ì˜ÌÌÉ ÌÌZ̍ÌÉ œú>ðK̘̍̏Ì̍ÌÉ Í¥Ì¡ÉôQ̍ÌÉ* Fò­ÌÌ™ÌÌâ­sÌfÌ Í¥Ì­Ì˜Ì`¥Ìœâú ¨Ì²tÌÉ Fò•òÌâuÌœâú** (C.S.Chi)

USE FUL MEDICATIONS : 

USE FUL MEDICATIONS Ghritam Kwatham Vasthi Nasya Anjana Dhoopana

Pathya : 

Pathya ͏̏ÌŸ™ÌÌ͵̕ò¡ôÌ™ÌÌ©Ì zùŒÌï²tÌFêò²™Ì ²ÌϏ̭Ì:* ÌfÌOÌ¥™Ì²™Ì Ì™Ì²Ì: Ìë™ÌÌâOÌÌâ ̭̘ͥÌ`Ìƥ̜âú** ²ÌÙœúÌ ²Ì˜Ìsn÷Ì Ì̍ÌÌtyÌä —ÌEKÌsÌâ ZÌœúsÌÌ™ÌÙŒÌÌ:* ÍtÌÍuÌÍœú©Ì ˜Ì™ÌÜœúÌ©Ì Ìë™ÌÌâ`™ÌÌ Í¥Ì­Ì˜Ì`¥Ìœâú** ¡ô¨Ìٍ̲™Ì ²ÌtÌæ¡ô²™Ì ÌëÌO—ÌHò˜Ìُ̲Ìâ¥ÌÌÉ* ˜Ì⌙Ì̍Ì̘ÌÙ­sÌ¥ÌÕ™ÌÌÊsÌ̘ÌÌ̭͘ÌÌsÌÌfÌ —ÌEKÌs̘ÌÆ** (C.S.Chi)

THANK YOU : 

THANK YOU