Department of Roga Nidana,

Govt. Ayurveda College

Kannur, Pariyaram

Faculty
Dr. R. Sreekumar MD (Ay)
H.O.D & Reader in charge of Professor

Dr. S. 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
 HYPERTENSION
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 Causes-
1. 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

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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.
Chronic arthritis
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.

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 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 Prithwi-
Dhriti, 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
DR. NARESH

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.

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 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 dosha-
sodhana 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…………

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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
MARASMUS
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
RICKETS
* Head-macrocephaly* sweats easily* fontenella – slow closing* skin – pasty looking
* Thorax- ricketic rosary* abdomen- disteded* legs – bow legs
PARALYTIC POLIO
Spinal form paralysis of legs (frog position) phantom hernia
BULBAR FORM
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
 SPINAL DISORDERS
DR. K.B.SUDHIKUMAR
Back pain may be due to Intrinsic or extrinsic reasons
Intrinsic causes-
1) Congenital - Spina bifida, Spondylolestheis.
2) Traumatic - Lumbosacral strain, IVDP, Vertebral fracture
3) Functional - Kyphosis, scoliosis.
4) Inflammatory – Arthritis, Fibrositis.
5) Degenerative – Spondylosis, osteoporosis
6) Neoplastic - Primary, secondary.
Extrinsic causes-
1)Abdominal – Pancreatitis, cholecystitis
2)Pelvic - Inflammation of ovary/tubes
3)Genitourinary - Renal calculi, prostitis.
4)Vascular - Ischemic from occluded arteries.
Psychogenic causes
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 signs- Shortened 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
Chronic
· 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 –
EòºªÉVɱɺªÉ+ɨÉÉƶÉƱÉÉÊiÉ<ÊiÉEòɨɱÉÉ**
EÖòÎiºÉiÉÆ+ɨÉƱÉÉÊiÉ<ÊiÉEòɨɱÉÉ**
• Lakshana sambandhi –
EòɨÉÆEòÉÏxiɱÉÖhÉÊiÉ<ÊiÉEòɨɱÉÉ**
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
Koshta Shakashrita
Haridra netra, twak nakha, mukha, Daha, Avipaka, Daurbalya, Anga sada, Aruchi, Durbala
indriyata, Balakshaya
Shakashrita
Haridra mootra, netra, twak, Sweta pureesha, Vishtamba, Gaurava, Parshva vedanam,
Hikka, Swasa, Jwara
TREATMENT
Kosta shakashrita Pittahara
Shakashrita Kapha vatahara

JAUNDICE
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
1. 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
1. Lids
Xanthelasma. White patches on the medial aspect, can be because of either DM or hyper
lipidemia.
Recurrent Stye.
Internal Hordeolum.
2. Conjunctiva
Telangiectasia.
Subconjuctival hemorrhage.
3. Cornea
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.
4. Iris
Rubeosis iridis.
5. Retina
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 Property-
Clots 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 Menorrhagia
o Metrorrhagia
o Polymenorrhoea
o Countinuous Bleeding Preceded By Amenorrhoea
Menorrhagia
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
Metrorrhagia
“Inter Menstrual Irregular Uterine Bleeding”
E G:- Carcinoma Of The Cervix Or Endometrium, Fibroid
Polymenorrhoea
Epimenorrhoea
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
Classification
* REGULAR (OVULAR)
* IRREGULAR (ANOVULAR)
Regular [Ovular]
Menorrhagia, Polymenorrhoea Polymenorrhagia
Aetiology
* 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
Avarana ……
• Srotas
• Anulomana
• Significance
• Definition
• Mechanism
• Diagnosis
• Classification
• Fate
• Complications
• Prognosis
• Treatment
• Avarana in Pakshaghata

SROTAS
Avyahata gati, Lives 100 yrs. With no disease
Srotodushti
Decrease in size
Increase in size
Anulomana
• 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
Retroviruses:
HTLV I : Adult T cell leukemia, lymphoma
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
Common Symptoms
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
IMAGING
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
Tumour markers
• 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
Radiotherapy: Role
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
Drugs Classified
Cell cycle dependent
Phase specific
Phase nonspecific
Cell cycle Independent
Chemotherapy
• 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
Chemotherapy: Drugs
 STROKE - DIAGNOSIS
DR. SUDEEP
-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.

H
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