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Gopakumar MD (Ay) Tutor P.G. Scholars Dr. K.S. Nandalal Dr. K.N. Ajithkumar Dr. Prabha. M. Kawna Dr. Sunil Babu P.P Dr. Madhu P.M Dr. S. Gopikrishna Dr. Mukesh E Dr. Viswanath K Dr. Preetham Pai Dr. Shobha Bhat
CONTENTS 1. CLINICAL RELAVANCE OF DASAVIDHA PAREEKSHA DR. R. SREEKUMAR 2. HYPERTENSION DR. BALAKRISHNAN VALLIOT 3. RADIOLOGICAL FINDINGS IN ARTHRITIS DR. MAHESH 4. ELECTRO CARDIOGRAM (ECG) DR. AJITH KUMAR M.K 5. CLINICAL RELEVANCE OF AGNI DR. K. MURALI 6. NON - TRAUMATIC DISEASES OF THE SHOULDER JOINT DR. NARESH 7. SAMPRAPTHI Vs SAMPRAPTHI VIKHATANA DR. GOPAKUMAR .S 8. CEREBRAL PALSY DR. T.K.UMA 9. SPINAL DISORDERS DR. K.B.SUDHIKUMAR 10. ENTAMOLOGY - ENVIRONMENT AND DISEASE DR. VENUGOPALAN. A.K 11. KAAMALA - DIAGNOSTIC APPROACH DR. R. SREEKUMAR 12. OCULAR MANIFESTATIONS IN SYSTEMIC DISEASES DR. SREEJA SUKESAN 13. DYSFUNCTIONAL UTERINE BLEEDING DR. RASIYA MONY 14. CONCEPT OF AVARANA DR. MANOJ KUMAR A K 15. FUNDAMENTALS OF ONCOLGY DR. V N BHATTATHIRI 16. STROKE - DIAGNOSIS DR. SUDEEP
Desam - Bhoomi & Athura desha: Here bhoomi pareeksha is about the land in which the patient lived. Athura desha pareeksha is the DASHA VIDHA ATHURA PAREEKSHA. Kalam - Samvathsara & Athuravastha: In samvathsara the 6 ritus are considered. In aturavastha ama-niramavastha, nava-puranavastha etc are considered. Pravruthi - Karma samarambha: Is the proper functioning of bhishak,aushada,atura & paricharaka. Upayam - Pada sampath: Bhishak,dravya,atura & paricharaka having all their required qualities forms the upayam. DASAVIDHA PAREEKSHAS Prakruthi: Some ualities which help to assess the various prakrutis are: KAPHA: Snigdhanga, Sukumara avadata gaatra, Sthira shareera, Manda chesta, Sheegra vikara, Prasanna darshana, Balavantha, Vidhyavanta PITTA: Ushna asha, Kshut pipasa vanta, Has more vali, palita,khalitya, Has less & kapila varna smashru, roma,kasha, Klesha asahishnu, Prabhuta ashana pana, Adhika swed, mootra,purisha etc VATA: Alpa shareera, Swara rooksha, jarjara, Chapala gati,chesta etc., Excess talk, P r o m i n e n t s i r a k a n d a r a , G r a s p s t h i n g s s o o n b u t f o rg e t s v e r y f a s t e t c , The knowledge of prakriti helps to assess: 1)The prognosis 2)Rogi bala 3)to know the mental status of the patient. Vikruthi: Here the changes taking place in the patients body must be noticed with due importance to: Hetu: the causative factor. ♦ Dosa. ♦ Dooshya ♦ Prakriti ♦ Desham ♦ Kalam By considering all these we can frame a proper samprapti of the disease, which in turn helps for proper treatment. Saram: The lakshanas of the 8 saras are watched out in the patient and a grading is done depending on the maximum qualities noticed as: PRAVARA, MADYAMA OR AVARA.SARA. Sara also represents the ojus or the bala of the patient. Samhananam: (compactness of the body) a compact body is characterized by symmetrical & well divided bones,well knit joints and well bound mamsa & rakta. Pramanam: Here the patient is examined with reference to the measurement of his bodily organs. this is determined by measuring the height, length & breadth of the organs by taking the finger breadth of the individual as the unit of measurement. Sathmyam: Satmya(homolagation)stands for such factors as are wholesome to the individuals.even when continuously used.. Pravaram - sarvarasa, ghritha, ksheera etc
DR. BALAKRISHNAN VALLIOT
-Leading cause of death in developed countries (70-75% of total deaths) -Hypertension is a hard pounding of blood and it exists in an adult when the brachial artery readings persistently exceed 140/90 mm of Hg. -Systolic pressure- Pressure exerted on the arterial walls when the heart contracts. -Diastolic pressure is the pressure exerted on the arterial wall when the heart relaxes. Increase in diastolic pressure would lead to aneurysm of the arteries and this condition cannot be treated efficiently. 300 billion-hospital visit • Increase in 33% from 1992 studies • 1/5 th above 160—65 • 50% in Framingham study 140/90 • 95% primary hypertension • 5% secondary hypertension • Urban India– 60/1000 • Rural India– 35/1000 • Increase in both areas MEASUREMENTS AND ERRORS • Sitting ideal, avoid drinks, smoking 30mts, rest for 5 minutes, mercury preferred, SBP and DBP to be recorded • 2-3 reading 1wk apart ideal, disappearance of korokoff phase 5 Potential errors in measurements • Inaccurate manometer, improper cuff size, arm not supported, not keeping arm at heart level, not taking SBP by palpatory, inflating/deflating fast, misinterpret auscultation gap Self measurement White coat HTN, assessment anti hypertensive, improving compliance, reducing cost RISK FACTORS • Smoking, obesity, dyslipidemia, diabetes mellitus, age more than 60 years, men, family history, woman more than 65, target organ damage, stress • Type A personality Secondary hypertension 1. Renal causes • UTI, renal calculi, polycystic kidney, AGN, liddle syndrome 2. Endocrine causes • Acromegaly, Cushing syndrome, Thyrotoxicosis, pheochromocytoma, Conns syndrome, hypothyroidism, PCOD, carcinoids 3. Drugs • Adrenalin, isporenalin, ephedrine, cyclosporin, carbenoxolone • Corticosteroid, erythropoeitin, ergotamine CLASSIFICATION A* 1) Systemic i. Primary or essential – unknown causes. ii. Secondary or where the cause is known. 2) Portal hypertension - i. Intra hepatic portal hypertension. ii. Post hepatic portal hypertension. iii. Pre hepatic portal hypertension. 3) Pulmonary hypertension - i. Primary (Unknown Causes) ii. Secondary (Known Causes).
PHYSICAL EXAMINATION • Polycythemia, radio femoral delay, vasculitis • Edema, Cushing, acromegaly, cardiomegaly, palpable kidney, bruite, AR murmur, collapsing pulse, retinopathy INVESTIGATION Urine, CBC, electrolytes, BUN, FBS, lipid profile, ECG, x-ray chest Optional Creatinine clearance, micro albuminuria, 24hr protein, uric acid, TFT, echocardiogram, test for secondary HTN DIAGNOSIS · Early diagnosis is essential. · Recording blood pressure routinely. · Investigations for the cause. DIFFERENTIAL DIAGNOSIS Common Causes1. Chronic pyelonephritis 2. Chronic glomerulonephritis. 3. Coarctation of aorta. 4. Renal artery stenosis. 5. Middle aortic syndrome. MANAGEMENT Drug therapy, diuretics, vasodilators, beta blockers, ace inhibitors, calcium channel blockers Supportive therapy life style modification, rest and relaxation, exercise, wt reduction programme, yoga & meditation Lack of response High cost, poor education, side effect of drugs, inconvenient dose, inadequate dose, poor compliance, concomitant drug use, Excess salt, alcohol, smoking, poor drug selection, co morbidity Hypertensive emergency Encephalopathy, ICH, AMI, IVF, eclampsia Urgency Unstable angina, diabetic nephropathy, pre eclampsia, drug intoxication COMPLICATIONS Related with affected parts- Heart, Brain, Kidney, Eye, etc. JNC VII
• • • • • •
50 years 140 SBP more risk than DBP Every 10/20 rise in BP double the risk Individual SBP 120-39 and 80-89 is pre hypertensive Thiazide diuretic is to be combined Many need two drugs to control Motivation improve compliance and stress given
ANKYLOSING SPONDYLITIS Usually occurs in younger individuals. X-ray findings are erosion of joint, joint narrowing, fusion and periostitis. Another common condition that we come across is periarthritis of shoulder joint. This includes supraspinatous tendonitis, rotator cuff injury, frozen shoulder and subacromial bursitis. X-ray findings are osteopenia, bony spur or osteophytes and soft tissue calcification. Joint space will be normal.
OSTEOARTHRITIS Usually it occurs in old age and in most of the cases it is monoarticular.the joints subjected to stress are mainly affected like hip , knee, ankle and wrist. X-ray findings are joint narrowing which is asymmetric , subchondral sclerosis and osteophytes. In chronic cases there will be late destruction of articular margins. RHEUMATOID ARTHRITIS Most common in younger females and is polyarticular. The most frequently involved joints are metacarpophalangeal joints, proximal interphalangeal joints and wrist . feet is more involved than hand. X-ray findings are soft tissue edema, osteopenia, erosions of joint margins, symmetric joint narrowing and fusion in some cases.
CLINICAL RELEVANCE OF AGNI
DR. K. MURALI
In the process of Srushti, the Panchamahabhootas are having the main role to create a body. So each mahabhootas are given some qualities for the creation, such as PrithwiDhriti, Jala- Samgraha, Thejus- Paka, Vayu- Vyuha, Akasha- Avakasha. In this, Thejus is having the role of Agni. As we know in our body the role of Thejus or Agni is mainly done in the Koshta as Pachaka Pitha with the help of distinct factors like Samana Vayu and Kledaka Kapha. In the conversion of food materials to a human body the agni plays a major role. So the Pachaka Pitha – commonly known as Kayagni acts on the food materials directly and it is first converted to Sara & Kitta. From that Sara the Bhoothagni divides the Bhoothas. It is absorbed to the body for the Dhathus by the effect of Dhathwagni. This is postulated by three main nyayas like Ksheera dadhi nyaya, Khale kapotha nyaya, & Kedara kulya nyaya. In this stage some malas are formed inside the body. They are Kapha, Pitha, Kheshu malas, Sweda, Nakha, Roma, Sneha in netra, twak vit, & Ojus. The other malas excluding Ojus are excreted within intervals. As Ojus is termed mala it is not excreted. It is the mala of Sukla Dhathu & is retained in the body and is passed over to next generation through pregnancy. Coming to the importance of agni in the samprapthi of roga - the agni is having some vitiated properties like Vishamagni, Mandagni, & Theekshnagni. These agnees cause the indigesion of food causing Ajeerna. By the difference of agnees we are getting three types of Ajeerna. 1. Mandagni – Ama. 2. Theekshnagni – Vidagdha, 3. Vishamagni – Vishtambha The common symptoms of Ajeerna are: Vitbandha, athipravrithi, glani, moodha vayu, vishtambha, gourava, bhrama etc. 1. AMA There are various views about the concept of Ama a. Apakwa annarasa itself as Ama b. Formation of Ama from Dosha moorchana c. Formation of Ama from Mala sanchaya d. Formation of Ama in the early stage of Dosha dushti Definition of Ama: it is Avipakwa, Asamyuktha, Durgandha, Pichila In the primary manifestation of Ama with body we are getting some symptoms like srotho rodha, dourbalya, gourava, moodha vayu, alasya, ajeerna, nishteeva, vitbandha, aruchi, klama etc. In the secondary manifestation of Ama with different Doshas we are getting Saama Dosha lakshanas. If the Ama is manifested with Vatha dosha we get – Tandra, sthaimithya, gourava, snighdhathwa, aruchi, alasya, saithya, sopha, agnimandya etc. If it is with Pitha we get – Durgandha, haritha – syavatha, amla, amlika, hrith daha, etc. and If it is with Kapha we get – Avila, thandula, sthyana, durgandha, vibandha etc By this manifestation the doshas may be in an avastha called Utklishta (moving) or Anutklishta (non moving). Eg. In Rajayakshma (agnimandya – upalepa- srotho rodha – dhathu kshaya) In Arsas (vyadhi hethuka nidanas + agnimandya) In Athisara (utklishta – Ama) In Udara (sroth rodha in udakavaha srothus) In Amavatha (Ama in madhyama roga marga) In Prameha (error in Sara kitta vibhajana) So considering the treatment principles we have to give the most importance to protect the Agni. Eg. In Utklishta avastha we have to give Upeksha (negligence), Pachana & Upadrava chikitsa In Anutklishta avastha we have to give Pachana, Deepana, Snehana, Swedana, & Sodhana
NON-TRAUMATIC DISEASES OF THE SHOULDER JOINT
Shoulder pain is the most common musculoskeletal complaint in men & women over the age of 40 yrs. Common causes of shoulder pain: A) EXTRA CAPSULAR:
Rotater Cuff Lesions:
1) Supra spinatous tendonitis or tear: It results from impingement of the tendon on the acromion.It is charecterised by a painful arc on abduction of the arm which can be abolished by external rotation, as well as by local tenderness over the greater tuberosity & pain on resisted abduction. Partial tears are associated with identical symptoms & signs. In some case there is radiographic evidence of calcific deposits . rupture of calcific material into the sub acromial bursa occationly results in acutely painful gout like attack of inflammatory subacromial bursitis. Fluid aspirated from the bursa contains crystals of calcium hydroxyapatite. TREATMENT: Local injection of steroids. 2) Bicipital tendonitis: It can be recognized by pain & tenderness in the bicipital groove aggravated by resisted flexion of the elbow. 3) Infra spinatus tendonitis:it is associated with pain on resisted external rotation. 4) Subscapularis lesions cause pain on resisted internal rotation of the arm. B) ACROMIO-CLAVICULAR: It includes conditions like arthritis. C) GLENO HUMERAL:
CAPSULITIS/ FROZEN SHOULDER:
It is a common and disabling condition in which severe spontaneous shoulder pain is initially associated with capsular tenderness & painful restriction of all shoulder movemens & later with restriction of all shoulder movements alone. A frozen shoulder may be a late consequence of a rotator cuff lesion & sometimes follows a M.I, hemiplegia, herpes zoster, etc TREATMENT: With analgesics and local corticosteroid injection in the early phase, and mobilizing exercises after the pain has resolved. D) REFERRED: Cervical nerve root Ischemic heart disease Sub diaphragmatic pathology Polymyalgia rheumatica etc
SHOULDER HAND SYNDROME:
This syndrome is charecterised by burning pain, vasomotor changes, & severe limitation of the movement of the hand in association with restriction of the shoulder movements. A radiogtraph of the hand shows patchy osteoporosis after some weeks or months. TREATMENT: Is aimed at mobilizing the affected limb. Analgesics, a short course of systemic cortico steroids, sympathetic nerve block & physiotherapy can also be opted.
In sanga - of mild degree, dosha pachana is sufficientEg. Shadharana choorna in Amavatha. If sanga is of moderate or severe degree, Vathanulomana, koshtagamana and sodhana are the treatments.Eg. pithanirharana in Sakhashritha kamala. In athipravritti - SthambhanaEg. Kutaja in Athisara and Vasa in Rakthapittha. If atipravritti and sanga exists together, anulomana is the treatment Eg. Hareetakhi in Amathisara. In vimargagamana - srothorodhahara and Vatha anulomana chikitsa should be combined followed by shodhana e.g. gomoothra hareetaki in udara. In siragranthi, soshana is the treatmentEg. Guggulu panchapala choorna in varicosity. VYADHI - AVASTHA In Amavatha, first treatment is for Ama by langhana, swedana , deepana etc.It is followed by treatment for Vatha by snehana, virechana and vasthi. In vatharaktha - acute stage (Utthana) – lepana, abhyanga, parisheka should be done. Vatha - fluctuation in joint swelling – Nagaradi lepa – Bala taila. Pittha - tenderness in joints - Jatamayadi lepa - Pinda taila. Kapha - stiffness of joints - Kottamchukkadi lepa - Kottamchukkadi taila. In Gambheera Vatharaktha- snehapana, virechana, and vasthi are the treatment, which is followed by rasayana- Vardhamana pippali or Chyavanaprasha. In Amavatha and Vatharaktha Vatha is the main dosha hence vasthi is the main treatment but vasthi is different in both occasions i. e. Kshara vasthi in Amavatha and Ksheera vasthi in Vatharaktha. In Amavatha itself if vatha is more, Kshara vasthi is done with Ksheera and if kapha or ama is more Kshara vasthi is done with gomoothra. In Athisara, with blood and mucous – Ksheera prayoga or Piccha vasthi which is applicable to conditions related to ulcerative colitis also. All the treatment in arshas should aim vathanulomana and that is why almost all arshohara drugs contain hareetakhi, which is best Vatha anulomana Silajathu with chedana, and kiedasoshaka property is a drug of choice in peripheral vascular disease as Rasayana. Generally when ojus is to be enhanced Rasayana is the right measure after doing the sodhana. In manasikarogas along with vitiated thridoshas Rajus and Thamus are to be normalized by Harshana,Santhwana,and other forms of Daivavyapasraya chikitsa and Sathwavajaya chikitsa. UNEXPLAINED DISEASES IN AYURVEDA - APPROACH 1) Identify the signs and symptoms 2) Understand the doshas involved 3) Realise the modern pathogenesis 4) Apply the dosha-dooshya concept 5) Formulate a new samprapthi 6) Derive the treatment principle as per the new samprapthi 7) Do the upasaya to test the hypothesis 8)Make changes if needed.
How to win the battle?
Use the right tool at the right time as discussed above. In Alpadosha-langhana,in madhyadosha-langhana and pachana,in prabhootha doshasodhana is the general principle.Apply it according to the situation. CONCLUSION To be an effective physician… 1) Read the screenplay of the disease very well 2) Identify the important scenes 3) Anticipate the turnings and climax 4) Select the proper artists and technicians 5) Now it is the time for ACTION… You are starting the BATTLE against SAMPRAPTHI… Best of Luck…………
DIAGNOSTIC METHODS Delay in attaining motor milestones persistance of moros grasp persistance of primitive reflexes after the age of three months Crippling Feeding difficulty Drooling Bad teeth Constipation Behavioral problems etc. CT scan reveal areas under developed, ABNORMAL CYSTS MRI – gives better pictures of abnormal areas ULTRA SONOGRAPHY – used in infants before the closure of skull bones,to detect cysts and structures in brain EEG – to detect brains electrical activity that suggest a seizure disorder DIFFERENTIAL DIAGNOSIS * PSEUDOMUSCULAR DYSTROPHY * KWASHIORKOR * MARASMUS * RICKETS * POLIO MYELITIS * PSEUDOMUSCULAR DYSTROPHY DIAGNOSTIC METHODS * Difficulty in standing, walking, climbing stairs, arising from the pelvis * Gower sign – succession of movements involving arising from bed to an upright position. The child appears to be climbing up in his own thighs * Remarkable bulky calf muscle * Waddling gait
Infantile atrophy in early age. Remarkable wasting of muscles and subcutaneous fat, face is wizened and shriveled Irritable and hungry in the early stage.
* LATE STAGE
Refuses food Becomes miserable and apathetic Late walking due to lack of energy
* Head-macrocephaly* sweats easily* fontenella – slow closing* skin – pasty looking * Thorax- ricketic rosary* abdomen- disteded* legs – bow legs
Spinal form paralysis of legs (frog position) phantom hernia
Paralysis of muscles supplied by cranial nerves (dysphgia, nasal speech, dyspnoea, facial paralysis), mild hypertension
BULBOSPINAL – combination of both bulbar and spinal ENCEPHALITIS – changes in sensorium, irritability, drowsiness, unconciousness
PREVENTION Vaccination to the mother in pregnancy Better antinatal,natal and postnatal care Adequate neonatal care A special serum after each child birth to avoid rh incompatibility
Back pain may be due to Intrinsic or extrinsic reasons
1) 2) 3) 4) 5) 6)
Congenital - Spina bifida, Spondylolestheis. Traumatic - Lumbosacral strain, IVDP, Vertebral fracture Functional - Kyphosis, scoliosis. Inflammatory – Arthritis, Fibrositis. Degenerative – Spondylosis, osteoporosis Neoplastic - Primary, secondary.
1)Abdominal – Pancreatitis, cholecystitis 2)Pelvic - Inflammation of ovary/tubes 3)Genitourinary - Renal calculi, prostitis. 4)Vascular - Ischemic from occluded arteries.
SPINA BIFIDA Congenital defect in the posterior bony wall of the spinal canal involving the lacunae. Spina bifida occulta, Meningocoel, Meningomyelocele, Syringomyelocele, Myelocele - Most common
Spina Bifida Occulta - It is the improper fusion of neural arches
No protusion of cord or membrane, No projection on surface, Impairment of nerve function may be caused in some such cases by tethring of the dura, and through this the spinal cord, to the skin surface by a fibrous membrane. - Clinically, the common manifestation of nerve involvement is muscle imbalance in the lower limb-foot drop, backache. SPONDYLOLISTHESIS -Deformity of lumbosacral region produced by gradual slipping forward of luimbar spine over sacrum. -Four varieties 1)Spondylolitic - familial - spondylolysis in pedicle. 2)Congenital – superior facet defect. 2)Degenerative - Degeneration of facet joint and disc L4 L5 3)Traumatic - Hyperextension injuries (Fracture of pedicle).Nerve root may be compressed by the defective narrowed intervertebral foramina. CLINICAL FEATURES Back ache Gradual onset long duration, Usually intermittent, Aggrevates after exercise, Movements - restricted Physical signsShortened trunk, Deep transverse furrows, Prominent sacrum Lordosis X-ray - AP – 5th transverse level with upper border. Lateral – Ullman’s sign, Oblique LUMBOSACRAL STRAIN Commonest variety of acute back ache, usually caused by strain, stretching or tearing of ligaments Lumbosacral joint is forced beyond the normal range of movement. CLINICAL FEATURES · Localised pain and tenderness · All movements restricted. · Rarely radiates
· Occurs in individuals with poor musculature · Insidious onset
ENTAMOLOGY - ENVIRONMENT AND DISEASE
DR. VENUGOPALAN. A.K
TYPE OF MOSQUITOES & DISEASES TRANSMITTED Anopheles - Malaria, Filaria (not in India) Culex - Bancroftian filariasis, Japanese encephalitis, West Nile fever, Viral arthritis (epidemic / poly arthritis) Aedes - Yellow fever (not in India), Dengue, Dengue haemorrhagic fever, Chikungunya fever, Chikungunya haemorrhagic fever, Rift valley fever, Filaria (not in India) Mansonoides - Malayan (Brugian) filariasis, Chikungunya fever Housefly - Typhoid, Paratyphoid fever, Diarrhoea, Dysentery, Cholera, Gastro- enteritis, Amoebiasis, Helminthic Infestations, Poliomyelitis, Conjunctivitis, Trachoma, Anthrax, Yaws .etc Sand fly - Kalaazar, Oriental sore, Sand fly fever, Oraya fever Tsetse fly - Sleeping sickness Louse - Epidemic typhus, Relapsing fever, Trench fever, Pediculosis Rat flea - Bubonicplague, Endemic typhus, Chiggerosis, Hymenolepis diminuta Blackfly - Onchocerciasis Reduviid bug - Chagas disease Hard ticks - Tick typhus (Rocky Mountain Spotted fever) Viral encephalitis (e.g., Russian Spring - summer encephalitis) Viral fevers (e.g., Colorado tick fever) Viral haemorrhagic fever (e.g. KFD in India) Tularaemia, Tick paralysis, Human babesiosis Soft ticks - Q fever, Relapsing fever, KFD Trombiculid mite - Scrub typhus, Rickettsial - pox Itchmite - Scabies Cyclops - Guinea- worm disease, Fish tapeworm (D. latus) Cockroaches - Enteric pathogens TRANSMISSION OF ARTHROPOD – BORNE DISEASES 1 DIRECT CONTACT e.g., Scabies and Pediculosis 2 MECHANICAL TRANSMISSION e.g., Diarrhoea, Dysentery, Typhoid, Food poisoning and, Trachoma by housefly 3 BIOLOGICAL TRANSMISSION PROPAGATIVE e.g., Plague bacilli in rat fleas CYCLO - PROPAGATIVE e.g., Malaria parasite in Anopheline CYCLO - DEVELOPMENTAL e.g., Filarial parasite in culex, Guinea worm embryo in Cyclops PRINCIPLES OF ARTHROPOD CONTROL 1 Environmental control 2 Chemical control 3 Biological control 4 Genetic control MOSQUITO CONTROL MEASURES
Anti - larval Measures
Environmental Control Chemical Control Biological Control
Anti - adult Measures
A) Residual Sprays B) Space Sprays C) Genitic Control
KAAMALA - DIAGNOSTIC APPROACH
DR. R. SREEKUMAR NIRUKTHI • Nidana sambandhi –
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• Lakshana sambandhi –
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BHEDA • KOSHTA SAKHASRITHA (BAHU PITHA KAAMALA) • SAKHASRITHA(ALPA PITHA KAAMALA) NIDANAS – KOSHTA SAKHASRITHA • Pithaprakopa Nidanas Madya, Amla lavana athibhojanam, etc.. • Raktha prakopa Nidanas Dadhyamlam, masthu, suktham, virudhanna, poothi anna etc. Causes Pitha and Raktha vitiation NIDANAS - SAKHASRITHA Rooksha, Sheetha, Guru, Athivyayama etc..Vatha and Kapha vitiates SAMPRAPTHI Koshta Sakhasritha • Pitha prakopa nidanas, Agni dushti & pitha dushti, Agni mandya & amotpathi Circulation of Saama dosha with Raktha, Raktha vaha srotho dushti, Adhika raktha mala utpathi, Circulation of Raktha mala with Raktha, Raktha Mamsa dushti, Kaamala nirvrithi Sakhasritha • Kapha & Vatha prakopa nidanas, Agni mandya, Amotpathi & dosha vridhi, Pitha marga gamana, Mala ranjaka pitha margaavarodha, Vatha prakopa & vimarga gamana of Pitha, Kaamala nirvrithi LAKSHANAS
Haridra netra, twak nakha, mukha, Daha, Avipaka, Daurbalya, Anga sada, Aruchi, Durbala indriyata, Balakshaya
Haridra mootra, netra, twak, Sweta pureesha, Vishtamba, Gaurava, Parshva vedanam, Hikka, Swasa, Jwara TREATMENT Kosta shakashrita Pittahara Shakashrita Kapha vatahara
It is a symptom complex charecterised by the yellow discolouration of the skin, sclera, mucous membranes & other tissues due to exess of bilirubin in the blood. In simple words it is the disturbance in the synthesis, manufacture, secretion or excretion of bile. NORMAL BILE PIGMENT METABOLISM
1) BREAK DOWN PHASE:
Haemoglobin break down occurs in the reticulo endothelial system forming the bile pigment bilirubin which is tranceported in the blood stream attached to albumin. This is not water soluble.
2) CONJUGATION PHASE:
Unconjugated bilirubin is lipid soluble & cannot be excreted from the kidney. For elimination it is transportedto the liver, taken up into the hepatocytes, conjugated with
OCULAR MANIFESTATIONS IN SYSTEMIC DISEASES
Dr. SREEJA SUKESAN
DIABETES MELLITUS Retinal changes rarely develop in a diabetic (less than 3 years) Ocular changes seem to depend more upon duration rather than on the Inadequate control. Common age group is 50 – 60 and male-female ratio is 2: 3 Those who are having hereditary tendency are at risk. Structure Wise Ocular Lesions Are
Xanthelasma. White patches on the medial aspect, can be because of either DM or hyper lipidemia. Recurrent Stye. Internal Hordeolum.
Telangiectasia. Subconjuctival hemorrhage.
Decreased corneal sensitivity (Due to Trigeminal neuropathy) which may lead to trauma Punctate Keratopathy Higher incidence of infective corneal ulcers and delayed epithelial healing due to abnormality in epithelial basement membrane.
Characteristic Fundus lesion consists of: Dot & Blot hemorrhages – Exudates - Obliteration of Pre-capillary arterioles - Results in focal areas of Retinal anoxia. – Neovascularization – Vitreous hemorrhage - Retinal detachment - Increased Intra ocular pressure.
6. Lens: Cataract. 7. Vitreous: Vitreous hemorrhage - Fibro vascular proliferation. 8. Optic Nerve: Optic neuritis. 9. Extra Ocular Muscles: Ophthalmoplegia due to Diabetic neuropathy. 10. Changes In Refraction: Myopia - Decreased Accommodation.
2. HYPERTENTION The factors which play role in the pathogenesis of Hypertensive Retinopathy are – 1. Vasoconstriction Hyper tonus – followed by hypertrophy .Hyperplasia of tunica media 2. Arteriosclerosis 3. Increased Vascular Permeability Abnormalities in the fundus: · Attenuation of arterioles · Arterio venous crossing changes · Segmental calibre variation in the arterioles · Hemorrhage · Exudates Hard - in chronic hypertension Soft - in malignant hypertension · Papilloedema - malignant hypertension 3. DEMYELINATING DISEASES From ophthalmologic point of view three of them deserve special attention Ø Multiple (disseminated) sclerosis Ø Disseminated myelitis with optic neuritis Ø Diffuse sclerosis
DYSFUNCTIONAL UTERINE BLEEDING
DR. RASIYA MONY
MENSTRUATION The visible manifestation of the-cyclic -physiologic -uterine bleeding - out of shedding of the endometrium,-due to invisible interplay of hormones Mainly through -hypothalamo - pituitory ovarian axis. CONTENTS Dark Altered Blood, Desquamated Endometrial Cell Debris, Fragments Of Endometrium, Cervical Mucous, Vaginal Epithelial Cells, Calcium, Bacteria Blood Clots In Uterine Cavity- By Its Thromboplastic PropertyClots Are Dissolved By-The Fibrinolysinec - Released From The Endometrium
Dysfunctional Uterine Bleeding
Excessive Uterine Bleeding Where No Organic Cause [Systemic, Haematological Or Pelvic Can Be Detected
Nature Of Bleeding
o o o o
Menorrhagia Metrorrhagia Polymenorrhoea Countinuous Bleeding Preceded By Amenorrhoea
Excessive Menstrual Loss In Amount Or Duration Or Both Causing More Than 80 Ml Of Blood E G:-Fibroid , Ca Of Endometrium, Endometrial Hyperplasia,Pcod With Tonic Estrone And Lh Effect, Obesity With Tonic Estrone & Lh Effect,Hypothyroidism
“Inter Menstrual Irregular Uterine Bleeding” E G:- Carcinoma Of The Cervix Or Endometrium, Fibroid
Too Frequent Menstruation At Regular Intervals Of 2 Weeks But Less Than 3 Weeks Ø Can Be Normal In Amount Ø When Becomes Heavy -Epimenorrhagia Ø May Occur At Any Time Ø Temporarily Develop At Perimenopause, After Abortion And Child Birth
* REGULAR (OVULAR) * IRREGULAR (ANOVULAR)
Menorrhagia, Polymenorrhoea Polymenorrhagia
* No Menstrual Endocrinal Disorder • Excessive Endometrial Secretion Of Pge2 * Excess Prostacyclin In Endometrium & Myometrium • Excess Fibrinolysis With Failure Of Secondary Thrombotic Plug * Defect In The Spiral Vessels Endometrial Vascular System Affected By Sympathetic Nervous System
Irregular [Anovular ]
Seen In Puberty,Premenopause,Obesity ,Pcod ,Corpus Luteal Abnormalities AETIOLOGY
CONCEPT OF AVARANA
Dr. MANOJ KUMAR A K
TRANSPORTATION • Jalasandhanavat • Agnisandhanavat • Sabdasandhanavat
• • • • • • • • • • • •
Srotas Anulomana Significance Definition Mechanism Diagnosis Classification Fate Complications Prognosis Treatment Avarana in Pakshaghata
SROTAS Avyahata gati, Lives 100 yrs. With no disease
Decrease in size Increase in size
• All movements • All direction • For health • Dosha dhatu agni samatam…. SIGNIFICANCE Better patient management DEFINITION Avarana: Doshanam samsarga: • Avarana: gatinirodha: • Avarana: margarodha: • Avarana: sanga: EFFECT • Temporary condition • A disease DIAGNOSIS • Mode of onset • Symptomatology • Site of onset • No evidence of Dhatu kshaya CLASSIFICATION • Dosha • Dhatu • Anna • Mala • Mootra
FUNDAMENTALS OF ONCOLGY
DR. V N BHATTATHIRI What is Cancer ?
• Abnormal, uncontrolled growth of cells • Ability to invade adjacent structures • Produce metastasis • Is of self origin Disease of heritable, somatic mutations affecting cell growth and differentiation, characterized by abnormal, uncontrolled growth. ONCOGENESIS Multistep process 1 Gene mutation: genotoxic agents Activation of Oncogene Inactivation of suppressor genes 2. Alteration in Signal transduction Loss of cell cycle control No apoptosis 3. Acquire features of malignancy Immortal Greater growth Absent cell cell interactions invasion and metastasis CANTER——>CANCER
Growth of a tumour
Three phases to its growth. 1. Exponential phase: Nutrition from interstitial fluid. 1->2->4->8->16, etc. 2. Lag phase occurs: Insufficient nutrition Slow growth 3. Plateau phase Neovascularisation; Tr. VEGF Cell death too About 40 doublings to clinical size
Aetiological factors: Viruses
RNA and DNA viruses (retroviruses) Adenoviruses: Cell cultures transformed Hepatitis B and C: Hepatocellular carcinoma Herpesviruses: Epstein Barr (EBV) Burkitt’s lymphoma, Immunoblastic lymphoma Nasopharyngeal carcinoma KSHV (AIDS too): Hodgkin’s disease, Kaposi’s sarcoma, body cavity based lymphoma Papillomaviruses: Anogenital, upper airway cancers, Skin cancer Polyomavirus: Neural tumors, Insulinomas, Mesotheliomas
HTLV I : Adult T cell leukemia, HTLV II: Hairy cell leukemia
Aetiological factors: Chemicals
Genotoxic or nongenotoxic Tobacco: Many cancers Diethylstilbestrol: transplacental: Ca vagina in child Occupational carcinogens: vinyl chloride, benzene, aromatic amines, bis (chloromethyl) ether Dietary factors: enhance or inhibit
Gross type: Growth, ulcer or induration Invasion: Bleeding, ulcer, bone/cartilage necrosis Tr. secretions: Biochemical effects, functioning tumours paraneoplastic syndromes Nutritional effects: Cancer cachexia Secondary effects: Infection, fever
Growth or Ulcer: Oral cancer Hemoptysis, cough: Lung cancer Bleeding mole: Melanoma Haemetemesis: Stomach cancer Dysphagia: Stomach cancer Abdominal pain, ascites: Intra-abdominal tumours Head ache, vomiting: Brain tumour Persistent fever, anemia, weakness: Leukemias Swellings: Commonest; Lymphnode mets, lymphomas, breast cancer, sarcomas Vaginal Bleeding: cervical cancer Blood in stools: Colorectal cancer Hematuria: Bladder cancer Paralysis: spinal/vertebral tumours All these more often due to other causes INVESTIGATIONS • DIAGNOSTIC • STAGING • PROGNOSTIC • ASSESSMENT • TREATMENT EVALUATION Types - Imaging, Endoscopy, Tumour markers
Radiological: Commonest X-rays: Plain, Barium Swallow and meal, IVP CT Scan: Whole body spiral CT; Contrast MRI Scanning: Dynamic contrast enhanced brain, spine and head & neck Functional Imaging: PET; P M R Spectroscopy Ultrasonography: superficial; transrectal, transvaginal Radionuclide imaging, Machines: Gamma camera, SPECT Indirect or non-specific scans: Perfusion Bone, Liver Direct or specific: Gallium 67 Citrate Scans: Lymphomas, lung, high ferritin tumours Thyroid, Adrenal Endoscopy: Inspection and collection of cells by b i o p s y, s c r a p i n g , w a s h i n g , e t c . cytology, Video - endoscopies Nasopharyngoscopy Oesophagoscopy,Gastro-duodenoscopy Colonoscopy, Cystoscopy Laparoscopy, Colposcopy Bronchoscpy, Thoracoscopy, mediatinoscopy
• • • • •
Carcinoembryonic antigen: Stomach, colon, liver Alpha fetoprotein: Teratomas CA125: Ovary BetaHCG: Choriocarcinoma PSA: Prostate
Remote afterloading: Moderate and High dose rate machines
Action of ionosing radiation
Interaction with matter Physical: Ionise atoms Physicochemical: Free radical formation Chemical: Damage to DNA, Cell membrane Biological: Cell death: apoptosis or necrosis Affect tumour as well as normal tissues. In normal tissues unaffected cells repopulate, but if unaffected cancer cells repopulate, tumour recurs. RADIOTHERAPY: COMPLICATIONS AND HAZARDS *Complications to patients High treatment doses Depend on site/organ/tissue as well as volume of tissue irradiated Proliferating: Easily damaged; repairable Mucositis, dermatistis, diarrhoea, etc. Non-Proliferating: Resistant, permanent Fibrosis, necrosis Radiation hazards to staff: Risk of Germ cell damage Risk of somatic cell damage: Cancer
Limitation: Number of tumour cells, disease extent RT as single modality: Many solid tumours Head & neck cancers, Cervix, Oesophagus, Early Hodgkins Disease Part of Combined modality Breast, Lung, Many Advanced solid tumours Palliative: Pain relief: Bone mets, Brain secondaries
Surgery: Limitation: Extent of tumour
Simple excision and closure Resection and plastic repair Resection and anastomosis
Morbidity: Cosmetic: Plastic repair
Loss of function: Prosthesis Surgery: Role in Skin, Head & neck cancers, Breast, Lung, Salivary gland, Stomach, Intestines, Brain, Soft tissues, Uterine, ovary, Kidney, Prostate
Chemotherapy: Use drugs
Limitation: Number of tumour cells, but not extent
Cell cycle dependent Phase specific Phase nonspecific Cell cycle Independent
• • • • •
Single drug or Combination chemotherapy Route Systemic Intra-arterial: Tr perfusion Intrathecal: into CSF Instillation: Bladder Intra-cavitary: Pleural, peritoneal Single Modality Combined Timing Neoadjuvant Concurrent with radiation Adjuvant
STROKE - DIAGNOSIS
-Stroke is one of the leading causes of the death and disability throughout the world. -It is rapidly developed clinical signs of focal or global disturbance of cerebral function; lasting more than 24 hours or leading to death, with no apparent cause other than vascular origin. The 24 hours threshold in the definition excludes transcient ischaemic attacks(TIA). -The disturbance of cerebral function is caused by three morphological abnormalities, i.e. stenosis, occlusion, or rupture of the arteries. RISK FACTORS Hypertension, cardiac abnormalities e.g. left ventricular hypertrophy, diabetes, elevated blood lipids, obesity, smoking, blood clotting and viscosity, oral contraceptives, etc. -Stroke includes a number of syndromes with differing aetiologies, prognosis and treatment e.g. Subarachnoid hemorrhage, Cerebral hemorrhage, Cerebral thrombosis or embolism, Occlusion of pre cerebral arteries, TIA, ill defined cardiovascular disease, etc. Dysfunction of the brain manifests by various neurological signs and symptoms that are related to extent and site of the area involved and to the underlying causes. These include coma, hemiplegia, paraplegia, monoplegia, multiple paralysis, speech disturbances, nerve paresis, sensory impairment, etc. PROGNOSIS there is and enormous variation in the prognosis for stroke depending upon the presence or absence of continuing risk factors. INVESTIGATIONS · CT Scan – Seen as areas of low attenuation. · MRI- as zones of high signal. · Angiography. · Arteriography.
Dr Pretham Pai Kulyadi house Kadbattu, Udupi, Karnataka; Pin – 576101 Ph – 0820 2521489 Dr K Shobha bhat, KRISHNA KRUPA, Chantar, Brahmawar, Udupi, Karnataka, Ph – 0820 2560815 Dr. S Priya Tutor, Govt. Ayrveda college, Trippunithara Ernakulam SREEVAS Palace road, Vakkam P.O Thiruvananthapuram. Pin – 695308 Ph – 04702 654368 Mob – 9847390543 Dr. Sanila V.K. Pallikkulam, Chirakkal P.O Knnur Pin - 670011 Ph – 04972746619 Dr M Jayaraj Jaya nivas, Thiruvizha junction (NH) Mahithara market P.O Cherthala, Alappuzha. Pin – 688539 Ph – 0478 2814259, 94472 91152 Dr P Mohanan, Padmalayam, Irinav P.O. Kannur Pin – 670301 Ph – 0497 2867373 (res) Mob – 9447448956 Senior physician, Asoka pharmacy, Kannur – 1 Ph – 0497 2707112, 2712696
Dr Ebey Abraham Moongamakel Payam P.O. Edoor, Kannur, Ph – 0490 2450398 Mob – 9847853991 Arya Vaidya Sala ( Publications) Kottakkal P.O. Malappuram, Kerala Ph – 0483 2742226 Dr V. Thrivikraman, Veluthat mana Kavanchery P.O Mangalam, Tirur. Pin – 676561 Ph – 0494 2566212 Arya Vaidya Sala Kottakkal P.O. Malappuram, Kerala Ph – 0483 2742216 Dr.Mini.K.V Tutor, Nangelil Ayurveda College, Kothamangalam Nangelil House, Pulluvazhi P.O Perumbavoor, Ernakulam Dt. Ph: 9847314407 Dr.Sreekala Nambiar, Meleth House, Near Olachery kavu Talap Kannur 670002 Ph: 0497 2700748. Dr.Anija S. Aiswarya, Mangalamkunnu, Palakkad – 679514 Ph: 0466 – 2260131 Mobile : 9847673808. Dr. Shini K.K Shinshal, Maruthonkara P.O. Kavilumpara Via Kozhikkode 673513 Ph: 0496 2565182 Mob: 94474 70199
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