Acute Myocardial Infarction PPT


 

ACUTE_MYOCARDIAL_INFARCTION

CLICK LINK ABOVE FOR THIS POWER POINT FILE

Cardioprotective Effect of Parawata Shakrit (Fecal matter of Pigeon)



 

Cardioprotective Effect of Parawata Shakrit(Fecal matter of Pigeon) in Isoprenaline induced Myocardial Ischaemia in Rabbits.

Cardioprotective Effect of Parawata Shakrit

                                      Click  Above Link To Read full content

CLINICAL PERSPECTIVE OF AVARANA


CLINICAL PERSPECTIVE OF AVARANA

Prof. Dr. S.N. Ojha
Click follow this Author on Facebook
Avaran

Lecture on Avaran

Shabda Vyutpati

‘Aa’ upasargapurvak

‘Vru’ dhatwatmak

‘Lyut’ pratayatmak

Shabdakalpadrum explains vyutpati of Avarana shabda from ‘Vru’ sanskirt dhatu which means valayita, vestita, ruddha and samvita

Nirukti

According to Ayurvediya shabdakosha the word avarana means avarodha gatinirodha ie. obstruction or resistance or friction to the normal gati of vata. Vata dosha is the gatyatmak dravya within the sharir. Hence its normal gati is hampered or vitiated thus vata becomes avrita.

          Shabdakoshkar says that balwan dosha due to its vitiation impedes the durbala dosha and hampers the normal gati of the avrita dosha.

Vaidyak Shabdasindhu says avaraka means achchhadaka while avrita means achchhadita.

Charak in context of madhumeha (C.Su. 17) has used the word avrita gati; Chakrapani explains it to be ruddhagati.

Dalhan commenting on the word avritamarga (Su.Sa.2) explains it to be pratibadha marga while Chakrapani commenting on the same word in ashtauninditiya adhyaya explains it to be avarudhagati.

In context of Kasa; Chakrapani says pratighat means avarana while in context of shotha says badhamarga means avritamarga.

Thus the word avarana can be understood as;

Achchhadan

Avaruddha gati

Sanga

Pidhan

Samvaran

Aakirya

Prachadana

Vestana

Valayana

Pravrita

Samvrita

To understand avarana firstly we need to understand the Gati-sidhant explained by our acharya.

GATI SIDDHANT:

          C.Chi. 28/4

Avyahatgati explains the normalcy of vata dosha and whenever vata dosha remains in prakritawasta the person lives a healthy life for hundred years.

Chakrapani commenting on the word avyahatgati has used 2 significant words aparityakta swamarga and anavritamarga.

Above, we have already discussed what do we mean by avritamarga; resistance to the normal gati of vayu. Whenever there is absence of resistance to a object, it moves in its own marga, srotas, dhamani etc. this is known as avyahat or prakrita gati.

Parityaktamarga means the sharir dravya is unable to maintain its swamarga. Vimarga is a synonymous word for parityaktamarga.

All the dosha have a normal shakha kostha gati which when maintained, dosha are able to maintain there normal function.

Vata dosha is raja guna dominated; it is the one which gives the initiating force (preraka) for the movement of all the other dosha. Hence its gati is very significant. If vata dosha gets avrita or vimargashrit, various disease proces begins within the body.

C.Chi.28/60

Causes of vata prakopa is either due to dhatu kshaya or due to marga avarana.

Pratibandha is the word used by Chakrapani in context of avarana. Vata has been explained to be sukshma-marganusari and preraka. Thus whenever movement of vayu through the suksma srotas is obstructed or the preraka karma is hampered the dravyabhuta vata dosha gets prakopita or vitiated.

Thus whenever avarana will take place it means it will hamper the following karma

-         Vikshepa

-         Samvahana

-         Parivahana

-         Chavan

-         Pargamana

-         Sravana

-         Visyandana

-         Ativedana, etc.

Charak in Vividhaashitapitiya adhyaya says that along with healthy food; jatharagni, anupahata dhatushma, anupahata srotas and anupahata vayu are responsible for healthy life.

Chakrapani says dhatu themselves are nutrient for the other dhatu and the urja of sharirdhatu depends upon anupahatadhatushma, dhatuposhak rasavahi vyanrupamarita and dhatuposhak rasavaha srotas

Anupahata dhatushma:-

Charak explains jatharagni is the one which gives bala to bhutagni and dhatwagni. For complete conversion agni is needed. Unless and until complete conversion of ahar into dhatuposhakansa does not take place they are not assimilated; such improperly converted dhatuposhakansa are called as the aparinamit dhatu or sama dhatu which offers resistance to the normal gati of vata dosha.

Hence, homeostasis in the content of dhatuposhakansa is brought about by the dhatushma it is therefore said to be responsible for dhatu urja.

Anupahata marita or dhatuposhak rasavahi vyanrupa vayu.

Amurta, subtle but dravyatmak vata existence in the sharir is understood by its vikshepana karma.

Charak in grahanidosha chikitsaadhyaya explain vyan vayu to be responsible for the continuous vikshepan of rasa raktadhi poshakansa.

Whenever sama dhatu are formed they disturb the normal gati of vata. The normal force required by the vayu for the transportation of dhatuposhakansa is unable to carry-out its normal function. The gati is restricted and the poshakansa is not made available to the dhatu thus leading to urja hanan of the dhatu. This explains the significance of dhatuvahi vyan vayu or marita in context of sharir dhatu urja.

Anupahata srotas

Sushrut says whenever ‘kha’ vaigunya is made available to vitiated dosha sanga takes place leading to the utpatti of vyadhi

Kha vikruti itself explains that the swaroop of aakash mahabhuta in that specific area is change ie apratighat guna of aakash is reducd and pratighat is increased. Pratighat develops sanga and apratighat contributes in prasarana or circulation. At definite extent pratighat is required across the srotas to provide the ahara rasa to surrounding part, but it is a non significant or negligible or non recordable, occurs at fastest rate and do not interfere with apratighatatva which maintains the constant condition or homeostasis.

One can understand the role of srotas in context of kapha, pitta, raktadi dhatujanya avarana but is their any role of srotas in context of parasparavarana?

Vatakalakaliya adhyaya gives the solution. Although vata being amurta, asanghata, anavastita dravya, how does its prakopa prashama takes place? Kankayan rishi says the rukshata, laghuta, sheetata, darunata adi lakshana are seen in the sharir viz srotas which leads to the prakopa of amurta vayu while dravya pradhan in snigdha adi guna act on sharir viz srotas and do the prashama of vata dosha.

Thus srotas plays an important role in prevention of utpatti of any disease.

In nut shell we can conclude the above discussion as;

Paraspara Avaran

Vata dosha is the same everywhere but depending on karma and sthana we classify it into 5 types viz pran, udanadi.

All the 5 types interplay within themselves and maintain homeostasis for eg due to prayatna of udan assimilation function of pran vayu takes place; saman vayu later on absorb the ahar rasa from where it is transported throughout the sharir with help of vyan vayu. Excretion takes place with help of apana vayu. When they themselves hamper their own karma, utpatti of vatavyadhi takes place.

Acharya Vagbhat has given the dusti hetu and dusti lakshana of pranadi pancha prakar vayu.

Vatabheda Nidan Lakshana
Pranvayu RukshaVyayamaLanganaAtyahar

Abhighat

Adhwagaman

Vega udiran

Vega dharan

Chakshu adi indriyopaghataPinasaShwasaKasa

Hikka

Trishna

Udanvayu KshavathuUdgarChardi             Vega vidharanNidra

Ati guru padarth sevan

Ati bhara vahan

Ati rodhana

Ati hasya adi

Kanta udhwansaMano branshaChardiArochaka

Pinasa

Galagandha

Jatru-urdhwa Vikara

Vyanvayu Ati adhwaEkasthana asanaAti dhyanAti krida

Vishama chesta

Virodhi ahar sevan

Bhaya

Harsha

Vishada

PunstwahaniUtsahahaniBalabhransaChittotplawa

Jwara

Nistoda

Romaharsha

Angasudata

Kusta

Visarpa

Sarvanga vikara

Samanvayu Visham-aharAjirnaSheetaharSankirna Bhojana

Akalashayan

Akalajagaran

ShoolaGulmaGrahaniPakwa-aamashayaj Vyadhi
Apanavayu RukshaGuru annaVegavidharanAagat

Ativahan seva

Yanaatisevan

Aasana atisevan

Chakraman atisevan

Mutra pradoshaj vikarShukra pradoshaj vikarGudabhransaPakwashayagata Vyadhi

Vishesha sthan has been explained for each vayu prakar but at each cellular level we can understand their functional activity such as assimilation of pran vayu, excretion of apan vayu, circulation and transportation of vyan vayu agnisandukshan or digestion & metabolism stimulants of saman vayu and prayatna of udan vayu. The concept is important because in case of paraspara avarana some symptoms have been explained which are not specific to their sthan for eg in saman avrita apana hridroga has been explained. There is  interplay between gati of different vata prakar. In normal condition they help each other to carry out various function but when there gati gets vitiated due to above hetu the balwan vata prakar impedes the gati of other leading to paraspara avarana.

Chakrapani/ C.Chi. 28/205

Concept of avarana in case of mana

Mana has its utpatti from avyakta. Avyakta being trigunatmak by satkaryavad siddhant mana is also trigunatmak swaroop. While satva is understood as guna of mana, raja and tama are understood as manashika dosha.

Mahabhuta also have origin from triguna as explained by Sushruta in sharirsthan first adhyaya.

Aakash is satva bahul

Vayu is raja bahul

Agni is satva raja bahul

Aap is satva tamo bahul

Prithvi is tamo bahul

All the 3 viz satva, raja and tama in balance state help each other although they have opposite qualities.

Satva guna is gyan prakashak

Raja guna is pravriti mulak

Tama guna is apravriti mulak

Mana and Panchamahabhuta both have origin from trigunatmak prakriti hence ahar which is panchabhautik in swaroop has its impact on mana and mana which is trigunatmak has its impact on sharir which is panchabhautik in swaroop.

In Sharirik vyadhi we find manas dosha lakshana while in manasik vyadhi we find sharirik dosha lakshana for eg in udavarta vyadhi mano vikar may occur as upadrava swaroop while in unmada we may find chhardi, karsnya adi sharirik lakshana.

Activity of satva and tama depends on raja similar to sharirik dosha where vata is responsible for kapha and pitta activity. All the 3 have abhibhava between them which in prakritavastha helps to maintain homeostasis while in vikritavastha cause various manasika vikar.

Hence in context of mada, murchha, sanyasa apasmara and attatvabhinivesh avarana has been explained.

Concept of gatavata and avarana.

Dhatu can be classified into two types asthayi dhatu and sthayi dhatu. Asthayi dhatus are the ones which are dravaswaroop and undergoing conversion (parinam aapadyamananam) and they are being vikshepita from their mulasthan throughout the sharir (abhivahan) for the purpose of poshan of the sthayi dhatu. This parinaman and abhivahan prakriya takes place in marga which are known as srotas; hence marga is one of the synonym used for srotas alongwith sira, dhamani, rasayani, rasavahini, nadi, panthana, sharir chhidra, samvrita-asamvritani, sthan, aashaya, niketa, sharirdhatu avakasha.

Prakopita dosha have the capacity to further vitiate both sthanasta dhatu as well as margagata sharir dhatu.

          When prakopita vata vitiates the dhatu it is called as gata vata, means vata prakop with specific nidan occurs as initiative factor to interplay with specific dhatu or vitiated itself in specific sthan (Amashaya gata vata etc.). In this context specific nidan for each and every gata vata related diseases must be observed to clarify why vitiated vata goes to specific part of the body or to specific dhatu to develop kosthagata vata, raktagata vata etc. Here dhatu functions like dusya.

In case of avarana pitta, kapha, rakttadi dhatu play the role of dosha or initiative factor to hamper the gati of vata, which in turn lead to avaraka and avrita components of avaraka respectively.

Comparative study of dhatugata vata and avritavata

Raktagata vata

Raktavrita vata

Tivra rujaSantapaVaivarnyaKrushata

Aruchi

Arushim cha gatre

Bhuktashya stamba

Twak mansa antarjadaha & arti/vedanaRagayukta shothaMandala

                            

In raktagata vata, rakta dhatu gets vitiated by vata dosha leading to shoshan of rakta dhatu; thus raktadhatu is unable to carryout its normal function of jeevan,varnaprasadhan, mansa poshan etc. Vaivarnya is caused due to loss ofvarnaprasadhan karma, due to improper mansa poshan krishata is seen, tivra ruja is seen due to depletion of poshana (Ischaemic pain).

Hetu explained in vidhishonitiya adhyaya are responsible for quantitative increase of rakta dhatu which impedes the gati of vata dosha hence normal parivahan is hampered and stagnation takes place leading to sanga this is the reason why in rakta avritavata raga yukta shotha, mandala, local daha and vedana have been explained. It can be compared with urticaria or vasculitis wherein we find rashes, burning sensation, pain, wheel & flare like presentation.

Treatment

Considering treatment we see use of sheeta pradeha, virechan and raktamokshan as line of treatment in raktagata vata while we see vatarakta like treatment in raktavritavata, where in treatment is given to reduce the quantitative increase of rakta dhatu and also normalise the gati of vata dosha with the help of basti hence importance of basti chikitsa in vatarakta has been explained.

(Na Hi Bastisamam kinchit vataraktam chikitsitam) C.Chi. 29/88

Mansamedogata vata

Mansa avrita vata

Medo avrita Vata

Guru angaTudyate atyarthamDanda mustihatamShramika atyartham KathinaVivarna PidakaShothaHarsha

Pippilikanam cha

Sanchar

ChalaSnigdhaMriduSheeta sopha

Aruchi

Mansa meda dhatu have similar characteristic both being snigdha, guru, sthira guna pradhan which gets vitiated by ruksha, laghu and chala guna of vata leading to disorder called mansamedogata vata. Various myopathies can be included under mansamedogata vata specially Carnitine palmitoyltransferase deficiency in which severe pain with fatigueness is seen. Myasthenia gravis can also be considered in mansamedogata vata.

Mansa dhatu is formed when vayu, ambu, teja and rakta ushma together bring sthirata to the mansaposhakansa. Sthira, kathina are the gunas of mansa while lepana is the karma of mansa dhatu. Such mansa when opposes the gati of vata kathina pidaka and shotha is formed. Nodules and tumours are defined as the solid, raised and firm growth.

When ambu, snigdha guna along with the dhatushma acts on poshakansa a soft, snigdha meda dhatu is formed. When such medadhatu will obstruct the gati of vata dosha it leads to origin of snigdha, mridu, ambulatory shotha. Lipoma bullae can be understood in context of medasavritavata.

Mansa medas avritavata may also be a complication of prameha since mansa and meda are the avaraka along with kapha and pitta to develop avritavata in basti and in turn leading to madhumeha as in C.Su.17. It indicates when mansa and meda become more vitiated and cause more kleda genesis or become kledanvita, they lead to different micro and macro angiopathy related complication. Meda-avrita vata can be compared with Diabetic nephropathy.

Pippilikanam cha sanchar are the abnormal sensory positive phenomenon or it may be the late complication of microangiopathy.

Treatment

-         Virechan, niruha and shaman is the chikitsa sidhant for mansamedogata vata.

-         In case of mansa avrita vata swedan, abhyanga, mansarasa, kshira and sneha prayog have been explained which will regularize the gati of vata as well as create normal poshakansa.

-         Pramehagna, medogna and vatahara chikitsa have been explained for amavritavata or for adhyavata

Thus avaraka and avrita both are being treated.

Asthimajjagata vata

Asthyavrita vata

Majjavrita vata

AsthiparvabhedaSandhishool

Mansabalakshaya

aswapna

santata ruk

Ushna sparshaPidanan cha abhinandati

Sam-bhajyate

Sidhati (Depressed)

Suchivad vedana

VinamaJrimbha

Parivestana

Sholam tu pidyamane

Panibyam labhate saukhyam

Due to external injury or due to pressure the asthi majja dhatu gets deranged leading to pain mainly at ashti parva or at the level of joints. The pain is continuous and it may later on show periarticular muscular atrophy as its late complication. It can be collectively understood under osteoarthritis where in focal loss of articular hyaline cartilage is seen with simultaneous proliferation of new bone with remodelling of joint contour. (sclerosis).

In asthyaavrita vata asthikshaya is observed (decrease bone density) increasing the symptoms of pain along with chances of fracture. Eka sthana vridhi anya sthan kshaya is other sidhant which explain the concept of osteophytes Osteophytes may compress the nerves root causing tingling or suchivata vedana (entrapment or compressive neuropathy).

In majjavrita vata the majja dhatu impedes the gati of vata (nerve conduction) leading to the symptoms like vinama; pain etc. Diffuse bulging of cord may be considered as well spinal canal stenosis.

Treatment

In asthi majjagata vata bahya aabhyantar snehan are the line of treatment so lubrication is maintained at the joint and results in prakritisthapan of vata.

Mahasneha prayog has been explained in asthi majja avritavata.

Note that a common treatment is explained in both the avaran and gata vata clinically too we see that Compressive Neuropathy or compressive myelopathy occurs in both the condition.

Shukragata vata

Shukravrita vata

Kshipra munchati / badnatiVikriti janayed shukram

garbham cha

AvegaAtivega

Nisphalatwan


In shukragata vata shukra are formed but either the count is less or there is some anomaly with its structure. Hence along with early ejaculation there is also abnormality in the foetus. Anomalies caused by extra sex chromosomes or less sex chromosomes can be included under this group (Aneploidy or polyploidy).

In shukragata vata sperms are formed but the count may be reduced in viral Orchitis, TB, STD, Chemotherapy, Ionizing radiation and drugs in which testesterone levels remain normal. It may cause premature or delayed ejaculations and also may cause abnormality in the foetus.

In shukravrita vata immature sperms are formed which loose their forward movement activity. Ciliary dyskinesia (kartagener syndrome) can be included in this group. Since motility is reduced it leads to infertility. Y chromosomes microdeletions and POLG variants are increasingly recognised as a cause of azoospermia or oligospermia. Primary gonadal deficiency with low-testesterone and decreased spermatogenesis are the reason for infertility.

Patients with normal hormonal levels and low sperm count may be found in obstructive anomaly of vas deferens and epididymus.

Treatment

Harsha and annapan responsible to increase bala of shukra is given. Virechan is advice if the marga is obstructed followed by above treatment.

In shukravrita vata too virechan has been explained followed by shukra bala vridhikar ahar and aushada.

 

Annavrita Vata

Bhukte kuksho cha ruja

Jirne shamyati

Ahar when taken in excess the prokinetic movement is reduced and the ahar is not propelled forward leading to strech reflex. The pain of obstruction of hollow abdominal viscere is classically described as intermittent food related abdominal pain followed by remission is seen.

Treatment

Vaman, deepan, pachan and laghu bhojan are the line of treatment.

Vaman causes gastric emptying thus avaraka is removed and with deepan, pachan aushadhi digestive capacity as well as vata gati is maintained.

Laghu bhojan is an important pathya which is followed in annavritavata

Mutra-avrita vata

Mutra apravritati

Aadhmanam cha basto

These symptoms are seen in mutra vega dharan. Normal urine formation takes place but the patient does not evacuate it timely leads to the avarodha of vata gati. Vata is unable to contract the detrusor muscle thus there is mutra apravritati and inturn bladder distension. This condition may also arise in neurogenic bladder.

Atonic bladder – Micturition reflex contraction cannot occur if the sensory nerve fibres from the bladder to the spinal cord are destroyed, thereby preventing transmission of strech signals from the bladder. When this happens, a person loses bladder control, despite intact efferent fibers from the cord to the bladder and despite intact neurogenic connections within the brain. Instead of emptying periodically the bladder fills to capacity and overflows a few drops at a time through the urethra. This is called overflow incontinence. Crush injury is the common cause.

Treatment

Swedan between bladder and nabhi pradesh alongwith uttarbasti

Purishavrita vata

-         Ati vibandha

-         Parikartika

-         Sneha ansa shigra pachana

-         Bhojan jirnortar aadhman

-         Shuska shakrit visarjan

-         Shroni, vankshana prishtha ruja

-         Viloma vata.

Dietary fibres adsorb water and this increases the bulk of stools and helps reducing the tendency to constipation by encouraging bowel propulsive movements. Diet low in fibres content reduces the healthy bowel movements. Stools are formed but due to slow transit there is hard and pelty stool formation which finds it difficult to pass out.

Malavega dharan may also cause the above symptoms. In Diabetes mellitus whenever there is neurogenic involvement, peristalsis are reduced creating the above symptom. Spastic colon may also be considered.

Treatment

Erandataila

Swedan

Udavartanashak Chikitsa

Treatment is given first to soften the stools and increase the intestinal motility so painless anuloman takes place.

Pitta avrita vata

Kapha avrita vata

-         Daha-         Trishna

-         Shoola

-         Bhrama

-         Tama

-         Sheeta kamita

-         Katu, amla, lavan,

ushna vidaha karak

- Shaitya- Gaurav

- Shoola

- Langhan, aayas, ruksha, usna kamita

- Katu adi upashaya karak

Due to intake of pittakar hetu quantitative vridhi of pitta takes place. It starts accumulating and now opposes the gati of vata which is unable to get rid off the pitta dosha so pitta vridhi lakshana are observed. Symptoms like daha etc are observed. The symptoms can be compared with heat stroke where the failure of heat regulating mechanism takes place.Giddiness, syncope may be observed, heat cramps may occur due to loss of sodium, potassium, chlorides in the blood. Hyperthermia reduces blood flow to brain causing giddiness.

While in case of Kaphavrita vata effect of cold stress should be considered. Muscular weakness is observed along with hypothermia. Symptoms may also arise in morning hours of cold seasons and rainy season. Working in air-conditioned rooms for longer hours can also create such symptoms. Even in common cold without pyrexia such symptoms may be produced.

Treatment:

The treatment is classified depending upon the sthan where the avarana takes place. Alternate shit & ushna in pittavrita vata.

If vitiated kapha and vayu are in aamashaya, vaman has to be followed, virechan is directed if it is pakwashaya sthita.

If pitta is vitiated throughout sharir virechan is adviced.

If by swedan kapha or the pitta reaches pakwashaya basti is to be adviced.

Gomutra is added in basti if kapha is involved while kshirabasti is given if pitta is involved.

Dhumpan and nasya is advice if kapha takes ashraya in shira pradesh.

After the shaman of kapha and pitta vatahar chikitsa has to be followed.

 

Pitta avrita pran

-         Murchha

-         Daha

-         Bhrama

-         Shoola

-         Vidaha

-         Shit kamana

-         Vidagdha anna vaman

Pran vayu is said to be controller, it helps in assimilation of ahar etc.

In pittavrita pran there is quantitative increase of pitta and it opposes the gati of pran, hence ingested food is vomitted out and since the ahar is not completely digested it comes out in the vidagdha form, as pitta has increased there are symptoms of daha, vidaha, murchha, bhrama and sheet kamana

Whenever food is ingested it stimulates the pharyngeal sensory receptors which send the impulse to the swallowing centre from where the motor impulses are sent with the help of 5th, 9th, 10th, 12th, cranial nerves to the pharynx and upper esophagus similarly sensory signals that initiate vomitting originate mainly from the pharynx, esophagus, stomach and upper portion of small intestine. The impulse traverses by both vagal and sympathetic afferent  nerve fibres to the vomitting centre from where motor impulse that cause vomitting are transmitted by way of 5th, 7th, 9th, 10th & 12th cranial nerves to the upper GIT causing vomitting. Thus vomitting may be initiated by nervous signals arising in the brain. Stimulation of the floor of 4th ventricle called chemoreceptor trigger zone with the help of administration of certain drugs initiate vomitting. If the gastric contents are incompletely digested are vomited out with a burning sensation associated with abdominal pain, vertigo, etc. Viral encephalitis may also be considered which is associated with high grade fever, focal neurological signs and seizures. These emergencies are difficult to treat so as said by Charak that pitta and kapha avritapran are difficult to treat.

 

Kapha avrita pran

-         Kshthivan

-         Kshavathu

-         Udgar

-         Nishwas Uchhwas sangraha

-         Aruchi

-         Chhardi

Vridha kapha opposes the gati of controller pran hence nishwas uchaswas karma are hampered at the same time chhardi, ksthivan and kshavathu symptom increases in frequency.

Depression of respiratory centre in the medulla should be considered.

Abnormal ventilation may be considered as in case of COPD where in mucus plugs prevents the gases exchange. The mucus accumulated in nasal and throat cavity obstructs the gati of pran causing irritation, the afferent impulses passes to the medulla where the reflex of kshvathu and ksthivam is triggered the same impulse also stimulates the vomitting centre causing chhardi.

 

Pitta avrita udan

-         Murchha

-         Daha, Bhrama

-         Nabhi Ura daha

-         Klama

-         Ojo bhransa

Karma of udan vayu is to generate urja, it is vaka pravritai mulak, prayatna balavarnakarak along with srotas prinan, dhi dhriti smriti mano bodhana are the karma of udan.

The pitta which has increased quantitatively along with its tiksna, usnadi guna are responsible for avaran of udan vayu. Thus prayatna, bala, varna nasha take place similar to the ojo bhransa explained by Sushruta, body gets fatigue as there is reduced energy and burning sensation between nabhi and ura along with murchha, daha bhrama adi vridha pitta lakshana.

As ATP production is hampered (Urja hani) metabolism gets hampered leading to GERD (Gastro Eosophageal Reflux Disease) causing heart burn and associated symptoms like fatigueness vertigo etc.

 

Kapha avrita udan

-         Vaivarnya

-         Vaka, swar graha

-         Daurbalya

-         Guru gatrata

-         Aruchi

Sheeta, guru, manda guna yukta vridha kapha has qualities opposite of vata. Especially when vitiated kapha impedes udan vayu, vaka pravritati, bala,varna, utsaha are loss thus creating the above symptoms. Panini has explained swarotpati in which he says atma and budhi come together and they give prerna to the mana which further stimulates vayu and it moves upward through the thorax cavity and with the help of astasthan helps in shabdhotpathi.

Vayu prakar which is moving in thorax cavity in upward direction should be understood as udan. Kapha obstructs this particular gati causing vakswargraha, thus muscular movement in larynx mouth and respiratory system does not occur in succession causing dysarthria.

As ATP is unable to generate energy, daurbalya and gurugatrata symptoms are enhanced.

Pittavrita Saman Kapha avrita saman
AtiswedaTrishna

Daha

Murchha

Aruchi

Upaghata ushma

AswedaGatranam cha atisheetata

Agnimandya

Roma harsha

Pitta gives ashraya for agni while saman is said to be agni uttejak bhava. When avaran of saman takes place abhava of agni uttejana occurs but it takes with the help of pitta hence we have sarvadaihik symptoms of pittavridhi with ushma upaghat. Hence we see excessive sweating leading to trishna associated with daha murcha aruchi which are pittavridhi samanya lakshana.

Zollinger Ellison syndrome may be understood in this case wherein gastrinoma secretes large amount of gastrin which stimulate the parietal cells of stomach to secrete acid to their maximal capacity.

Increase aldosteronism may also be considered under pittaavrita saman.

In kapha avritasaman the sheeta, manda guru guna obstruct gati of saman. Thus agni uttejak abhavata is seen leading to agnimandya. Difference between the above too is the excessive drava gunatmak vridhi which prevents agnivridhi in case of pittavritasaman while incase of kaphavritasaman the enzymes are absent and there is no conversion of ATP.

Pitta avrita vyan Kapha avrita vyan
DahaSarvanga klama

Gatra vikshepa sanga

Santapa

Vedana

GurutaAsthi sandhi peeda

Gati sanga

Vyan vayu is responsible for all gati, prasarana, aakunchana, utshepa, avakshepa, nimesha unmesha adi kriya.

Whenever avarana of vyan vayu takes place sanga or restriction of sarvanga gatra occurs & daha, santapa are the samanya lakshana of vridha pitta while guruta adi are samanya lakshana of vridha kapha.

Inflammatory myopathies may be considered under pitta avritavyan. Systemic features like fever and fatigue are common. Other systemic autoimmune disease such as SLE (Systemic lupas erythomatosis) or vasculitis can also cause myositis. Polymyalgia rheumatica may also be considered where in muscular pain and stiffness is present. There is no true vasculitis but there is close association with giant cell arteritis, fatigueness, fever and depression.

In case of kapha avritavyan fibromyalgia may be considered. In this disorder there is no structural, inflammatory or endocrine abnormality. Marked fatigability, pain along with signs of osteoarthritis is also observed.

Pittavrita apan Kapha avrita apan
Haridra Mutra / VarchaSantapa Guda / Medra

Raja atidarshan

Bhinna, Aama, KaphaSansrista guru varcha

Kaphaj meha

The quantitatively increased pitta offers resistance to the gati of apan. Role of apan is dharana of the sharir. Mala bhag is excreted out with the help of apan vayu, raja pravartan, garbha nishkraman are also functions of apan.

The vridha pitta imparts its haridra peetavarnato mutra and purisha. Due to its ushna and tikshna guna santapa is felt at guda or medra sthana. Pitta is mala bhag of rakta and rakta helps in poshna of raja dhatu. Both pitta and raja have samana gunadharma hence pitta vridhi also leads to raja vridhi causing raja atidarshan.

This condition may be compared with infective inflammatory changes in urethra, anorectum and vagina.

HSV (Herpes simplex virus )  increases vaginal discharge along with vulval pain and dysuria. In trichomoniasis infection there is vulva and vaginal inflammation along with froathy yellow / green discharge. HSV and trichomoniasis may also be responsible for proctitis and urethritis.

The snigdha, guru, pichchhila, drava guna yukta kapha has its resemblance similar to meda and kleda does the bahudrava kapha when gets basti prabhava and along with meda and kleda reach the mutravaha srotas and get settle at glomerulus (Aasadya pratirudyate gatwa awatistate) leading to utpatti of kaphaj prameha.

This condition can be compared with alimentary glycosuria, a rapid but transitory rise of blood glucose following a meal.The concentration exceeds the normal renal threshold; during this time glucose will be present in the urine.

Vridha kapha by its snigdha, pichchhil, aama swaroop, guna changes the consistency and physical appearance of the mala converting it into bhinna, aama, kapha sansrista guru varcha.

 

Prognosis of pitta and kapha avritavata prakar

-         Acharyas beleive  aavaran of pran and udan vayu by both kapha, pitta are a serious condition.

-         Anabhisyandhi, snigdha and srota shodhak dravyas should be selected.

-         Yapana basti with madhur rasa pradhan dravyas

-         Anuvasan basti

-         If patient is balwan mrudu anuloman is useful

-         Rasayan chikitsa to be followed

-         Shilajeet and guggulu should be administered along with milk

-         Chyavanprasa and abhayaamalaki rasayan should be given.

-         If apana vayu does the avarana then dipana grahi, vatanulomak and pakvashayashodhana dravyas should be selected.

-         In avarana due to pitta, therapy which alleviates pitta but does not work against vayu should be given.

-         If kapha does the avarana then therapies which reduce kapha and which do anuloma of vata should be selected.


Paraspara Avarana

Pran avrita Vyan

-         Sarva indriya soonyatwa

-         Smriti kshaya

-         Bala kshaya

Pran vayu acts like a controller. It is responsible for the aadana karma. Gyanendriya perceive their objects with the help of pranvayu.

Vyan vayu is responsible for gati or conduction. Hence vyan vayu plays a significant role in rasavikshepan. Conduction is not only related to cardiac cycle but all types of neural conduction should be considered.

Whenever the controller pran will restrict the gati of conducting vyan vayu the indriya will not be able to perceive its vishaya. It may happen in one indriya (homonymous) or in all indriya (heteronymous) together. If it happens in all indriya it can be compared with the vegetative stage or deep coma.

Rasarakta vikshepan is karma of vyan vayu. In case of eye; vascular disease related to retina / optic disc causes visual loss.

Alzheimers Disease may also be considered. Macroscopically, the brain is atrophic, particularly the cerebral cortex and hippocampus. Many different neurotransmitter abnormalities have been described in particularly impairment of cholinergic transmission through noradrenaline, 5 H-T, glutamate and substance P is also involved. Inability to retrieve information (smriti kshaya) is the symptom. Later apraxia, visuo spatial impairment and aphasia is seen.

Treatment – Urdhwa  jatrugata chikitsa.

 

Vyana avrita pran

Sweda atipravriti

Lomaharsha

Twak vikar

Supta gatrata

Sweda sravan is normal karma of vyan vayu thus whenever vyan gets vitiated it causes sweda atipravriti. It explains sympathetic overactivity or cholinergic effect. This may happen in anticholinergic side effects seen in poisoning. Sweat glands secrete large quantities of sweat when sympathetic nerves get stimulated. Visha is one of the hetu of vyan prakopa.

Perception is the function of pran vayu when it gets avrita its perception function is reduced. It is negative sensory feeling caused in disorders like diabetes mellitus

Excessive sweating may cause twakvikar due to dehydration.

Treatment

Sneha yukta virechan

Sneha helps to reduce vyan and virechan helps in bringing anuloma gati to pranvayu.

 

Pran avrita saman

-         Sharir jadatva

-         Gadgad

-         Mukata

Panini has explained that atma alongwith budhi activates the mana with the help of pran. Mana stimulates the kayagni with the help of saman vayu and gives prerna to vayu in upward direction which depending on ashtasthan produces various sounds. Thus vitiation of pran or saman leads to symptoms like gadgad and mukta.

Dysarthria, Mutism is associated with perisylvian region of left hemisphere. Posterior pole being Wernickes area and anterior pole of language is known as Brocas area. An essential function of this area is to transform neural word representation into their articulatory sequences so that words can be uttered in the form of spoken language. Both the poles are interconnected with each other and with additional perisylvian, temporal, prefrontal & posterior parietal regions making up a neural network subserving the various aspects of language function. Damage to any one of these components or to their interconnections can give rise to language disturbances (aphasia)

Treatment

Chatusprayoga sneha – gives bala to saman

yapana – gives bala to pran.

 

Udan avrita apan

Chardi

Shwas adi

In above condition we need to emphasize on gati of vata prakar. Udan has its urdhwagati while apan vayu has anuloma gati. In udan avrita apana; the later changes its gati and now becomes udan bhava aapana as commented by Chakrapani ‘Urdhwagati swabhava aapana’. Thus urdhwagati is increased causing symptoms like chardi, shwas etc.

Cigarette smoking often results in mucous gland enlargement and goblet cell hyperplasia. Goblet cell increase in number but in extent through the bronchial tree. Bronchi undergoes squamous metaplasia which disrrupts       mucociliary clearence leading to COPD.

Antiperistalsis means peristalsis up the digestive tract rather than downward. This may begin as far down in the intestinal tract as the ileum. It can push the contents upto duodenum and stomach leading to their over distention which becomes the exciting factor that initiates the actual vomiting act.

Treatment

Basti

Vata anulomak annapana

 

Apan avrita udan

-         Moha

-         Agnimandya

-         Atisar

Apan has it adogati and is responsible for kitta utsarjan while udan vayu is responsible for urja and has urdhwagati.

Apan when resist udan the udan vayu becomes apan bhava aapana. As udan vayu gets avrita urja or agni is reduced causing agnimandya. The increase kitta and reduced urja gives rise to moha and alpagni.

Uraemia may be understood in the above condition where the concentration of blood urea (kitta bhag) increases in blood.

Treatment

-         Vaman

-         Agnideepan

-         Grahi annapana

Agnideepan and vaman to increase bala of udan and normalize its urdhwagati and grahi annapana to compensate the vridha gati of apan.

 

Vyan avrita apan

-         Vaman

-         Aadman

-         Udawarta

-         Gulma

-         Arti

-         Parikartika

Apan vayu has to own anuloma gati and its role is to eliminate the faecal matter, urine etc.

In this avaran vyan opposes the gati of apan thus anuloman does not take place. Features resemble adovega dharan vyadhi like aadman, udawarta, gulma and vedana. When the person stresses while passing motions the hard stools cause painful condition called the fissure.

G.I. has its own intrinsic set of nerves known as intramural plexus or the intestinal enteric nervous system located on the walls of gut. Both parasympathetic and sympathetic stimulation originating in the brain can affect gastro intestinal activity mainly by increasing or decreasing specific actions in the gastrointestinal intramural plexuses. Strong sympathetic stimulation inhibits peristalsis and increases the tone of sphinctures. Net results in slow propulsion of food through tract sometimes decrease the secretion as well even to the extent of constipation. As the peristalsis are reduced the food remains in stomach or early part of small intestine which send the strech impulse to vomitting centre causing the vomitting.

Treatment

-         Snigdha anuloman

 

Saman avrita apan

-         Grahani

-         Parshwa / Hridgada

-         Aamashaya shoola

Saman vayu helps in agni sandukshan also it has role in anna dharan, pachan, vivechan and taking kitta downward.

Saman vayu is agni-samipasta vata prakar. Grahani avayava helps in apakwa ahar dharan and pakwa ahar is pushed forward in parshwabhag. In saman avrita apan vridha saman does not help in dharan of apakwa ahar. Grahani vyadhi is so called because grahani is unable to do dharan of ahar. As apakwa ahar moves forward parshwa shool begins.

Due to vitiated saman the number of intermediate metabolites increases and it obstruct gati of apan causing ischemia causing hridroga.

 

Treatment

Agnideepak ghrita

 

 

 

Pran avrita udan

-         Shirograha

-         Pratishaya

-         Nishwas Uchshwas sangraha

-         Hridroga

-         Mukhashosha

Role of udan vayu is to give urja, bala, increase prayatna, srotas preenan etc. They get hampered when pran does avaran over udan vayu. The pran vayu has adhogati while udan vayu has urdhwagati does mismatching takes place leading to sangraha of nishwas and uchshwas.

Failure of control over the immune system leads to autoimmune disorder. The above condition can be seen in rheumatic heart disease and also in allergic rhinitis.

Treatment

Aashwasan chikitsa

 

Udan avrita pran

Karma Nasha

Oja Nasha

Bala Nasha

VarnaNasha

Mrityu

Bala,varna, oja, prayatna depend on Udan vayu while controller and assimilator is pran vayu.

In udan avrita pran the pran gati is restricted does perceiverance and control is lost while udan vayu being prakopita oja,varna, bala nasha is seen.

The above symptoms are seen in terminally ill patient in which fatigueness and weakness is commonly seen associated with psychological symptoms like hopelessness, meaninglessness, confusion, delirium which are similar to oja nasha.

Underlying various disorders reduce the energy store. It occurs due to disease induced factors such as TNF, cytokines and from secondary factors such as cachexia, dehydration, anemia, infection hypothyroidism and DKA. Changes in muscle enzymes also plays an important role. RAS system may get involve later on causing semicoma followed by coma and lastly death.

Treatment

-        Shanaihi Sheetavarina Shinched

-        Ashswashan

-         Sukham cha upapadayet

 

Apan avrita vyan

Purisha                 Atipravriti

Mutra                             Atipravriti

Retasa                   Atipravriti

Karma of apan vayu is nissaran of purisha, mutra, artava and shukra at a specific interval.

Apan when gets vridha and restricts the gati of vyan the utsarga vriti of avaraka is seen. Thus atipravriti of purisha, mutra and retasa is seen.

There is interplay between gati of apan with gati of vyan. The srijan karma and gati karma of apan vayu vitiates vyan vayu which becomes avrita and thus rasa vikshepan karma is reduced.

Diarrhoea causes dehydration leading to reduced ventricular filling pressure. Modulation comes into play causing increase heart rate and peripheral vasoconstriction but if the dehydration continues the cardiac output is reduced thus leading to reduced rasa vikshepan causing hypovolaemic shock

Treatment

Sangrahan

Saman avrita vyan

-         Murcha

-         Tandra

-         Pralapa

-         Angaawasad

-         Agnimandyata

-         Oja kshaya

-         Sharir bala kshaya

Many systemic metabolic abnormalities cause altered sensorium by interrupting the delivery of energy substrates. Almost all instance of diminished alertness can be traced to widespread abnormalities of the cerebral hemisphere or to reduced activity of a special thalamocortical alerting system termed the reticular activating system (RAS). Suppression of RAS and cerebral function can take place incase of metabolic dearrangement such as hypoglycaemia or hepatic failure leading to stage of reduced comprehension, coherence and capacity to reason. Irrelevant talk, lack of appreciation of spatial relation of self or external environment (agnosia) may also occur.

Treatment

Vyayam

Laghu bhojan

 

Udan avrita vyan

-         Stabdata

-         Alpaagnita

-         Asweda

-         Chestahani

-         Nirmilan

Vyan vayu is responsible for gati, vikshepan, sweda sravan nimesha, unmesha etc. but whenever it gets avrita swa karma hani occurs and if it gets avrita by udan the one responsible for bala, prayatna, urja causes symptoms like stabdhata, alpagni, asweda, chestahani and nirmilan.

Continuous generalized electrical discharges of the cortex are associated with coma even in the absence of epileptic motor activity. The self limited coma that follows seizures termed the postictal state may be due to exhaustion of energy resources or effects of locally toxic molecules that are byproduct of seizures.

Treatment

-         Alpa and Laghu bhojan

Anukta Avaran

Vyan avrita udan

Vyan is associated with gati and prakshepan while udan is associated with bala prayatna & urja. Vikrut vyan has impaired gati which when impedes udan will reduce the bala, prayatna adi karma of udan.

Sympathetic fibres originate in the hypothalamus, pass down the brain stem and cervical spinal cord to emerge at T1, return back up to the eye in association with the internal carotid artery and supply the dilator pupillae. Lesion in the sympathetic pathway cause Horner’s syndrome. The reason may be central (at the level of Hypothalamus / brain stem) or at the periphery (at the level of lung apex, carotid artery) or may be idiopathic.

Vyan avrita udan can also be considered in paroxysmal tachycardia. Abnormalities in different portions of the heart including the atria, the Purkinje system, or the ventricles, can occasionally cause rapid rhythmical discharge of impulses that spread in directions throughout the heart. This is believed to be caused most frequently by re-entrant circus movement feedback pathways that set up local repeated self re-excitation.

The above process occurs unless considerable ischemic damage and may lead to ventricular fibrillation. Thus there is never a coordinate contraction of all the ventricular muscle at once which is required for cardiac pumping. Patient may complaint of palpitation or symptoms such as dizziness, dyspnoea, fatiguebility ie. Bala, prayatna are reduced.

Apan avrita saman

Apan is responsible for srijan karma. Vikrita Apan increases the nishkraman prakriya. Increase Hustration reflex causes excessive propulsion movement. Excess motility causes reduced absorption. The body in unable to reabsorb bicarbonate ions i.e. saman karma is reduced.

Loss of bicarbonate causes rise of H+. Body compensates the process by increased ventilation. The PaCO2 is reduced secondarily by hyperventilation which mitigates the rise in H+. Leading to metabolic acidosis

Diarrhea associated with passage of more than 200g of stool with urgency of defaecation and faecal incontinence. This may lead to malabsorption leading to hypoalbuminaemia, hypocalcaemia & vitamin D deficiency, hypomagnesaemia, phosphate , zinc and weight loss.

Pran avrita Apan

Pran vayu function is associated with controlling system of the body, as said by Nyayachandrikakar. Pran vayu helps in assimilation and maintain homeostasis

Apan is responsible for elimination. Considering pakvashaya it may be compared with srijan of purisha mutra etc. at cellular level considering removal of cellular products within the cell.

In this particular condition of pran avrita apan the vikrita pran obstructs the gati of apan and it is unable to release the cellular products. This can be understood in condition of Brainstem lesion where in the control over CO2 expiration is lost. Depletion of CO2 expiration leads to increase in concentration of CO2 in blood resulting in respiratory failure of Type II origin ie severe respiratory acidosis.

A simple sleep apnoea / hypopnoea syndrome may also be considered.

Udan avrita Saman

In this particular condition as udan vikriti takes place anabolism increase reducing the catabolism. This is observed in Hypothyroidism where in weight gain is seen with decreased appetite.

Leptin is secreted by adipose cells and acts primarily through the Hypothalamus. Its level of production provides an index of adipose energy stores. High leptin levels decrease food intake and increase energy expenditure. TheOBgene is present in humans and expressed in fats. The obesity in these individuals begin shortly after birth, is severe and is accompainied by neuroendocrine abnormalities. Role of central hypothyroidism has been understood in mouse model.

Another condition may be considered where increased acetylcholine stimulates increased ATP (­urja) which further increases excessive secretion of fluids and electrolytes in addition to normal viscid alkaline mucus which further increases gastrointestinal activity causing reduced absorption (annashoshan, vivechan karma) leading to malabsorption diarrhea.

 Vyan avrita saman

There is interplay between gati of vyan with gati of saman. Therefore when rasa vikshepan karma of vyan related to saman vayu is vitiated, the later becomes avrita and in turn annapachan, vivechan and munchan karma of saman are inhibited or decreased.

Sympathetic nerves have dual action in some cases. It increases secretion but if parasympathetic is already causing copious secretion sympathetic usually reduces the secretion mainly by vasoconstriction reducing the blood supply.

Although ENS (enteric nervous system) can function autonomously; ANS connects ENS centrally. When ANS activity is increased it has its impact on gastrointestinal tract.

Sympathetic overstimulation causes vasoconstriction which reduces secretion of gastric juices and pancreas exocrine secretion. Their insufficiency can cause malabsorption syndrome in which predominant feature is steatorrhoea, deficiency of fat soluble vitamins, protein and carbohydrate deficiency related features.

As compensatory mechanism vasodilatation in skin leads to excessive sweating and skin related features.

Saman avrita Pran

Role of saman along with agnideepan is to help in pachan and sara kitta vibhajan. Thus along with pitta, saman plays its major role in metabolism. If saman gets prakopit sara kitta vibhajan does not takes place properly and kitta bhaga gets upashoshit along with sara bhaga. Thus kitta munchan prakriya does not take place. This condition may be noted in metabolic acidosis, hypercalcemia and uraemia. The kitta bhaga now alters the gati of pran or in other words neuronal excitability. It may show symptoms like confusion seizures, coma and death. It may also depressed the respiratory centre causing hyperventilation or Kussmaul breathing.

 

Saman avrita Udan

The same kitta bhag depending on sthan obstructs the gati of udan. The bala, prayatna, urja adi karma are reduced.

Conditions can be observed in hepatic coma where in increase levels of ammonia (kitta bhag) interfere with cerebral energy metabolism and with Na+, K+, ATPase pump. Number and size of astrocytes are increased. They alter the nerve cell function and causes symptoms of fatiguebility, altered sensorium and coma. (prayatna nasha)

Similarly Hyperthyroidism may also be considered. Saman is said to be Agnibala pradha, it leads to increase in catabolism. Energy gets exhausted with increase catabolism reducing the bala prayatna which is the role of udan vayu as seen in thyrotoxicosis.

Apan avrita pran

Interplay exists between apan the eliminator and pran the controller of the body system. Mismatching between apan and pran karma leads to various disorders. If the srijan karma and gati of apan related to adan karma of pran gets vitiated the pran vayu gets avrita and in turn causing shwas, confusion, coma and death.

Loss of Na+, Cl-, H+ and extra cellular fluid depletion occurs in excessive administration of diuretics or in congenital chlorodiarrhoea. It leads to increase concentration of plasma HCO3 which leads to condition such as apathy, confusion and drowsiness.

In anxiety induced hyperventilation excessive loss of CO2 takes place. PaCO2 and H+ falls. The low PaCO2 results in reduced renal Na+/H+ exchange due to which patient feels short of oxygen.

A Holistic Approach to Geriatric Medicine


A Holistic Approach to Geriatric Medicine

Prof. Dr. S. N. Ojha 
M.D Phd

The word Geriatrics is made up of greek word called “Geron” meaning “old man” and “iatros” meaning “healer”vrudhha

Geriatrics is defined as department of medicine dealing especially with the problems of ageing and disease of elderly. It aims to promote health and to prevent and treat diseases & disabilities in older adults

The term itself can be distinguished from gerontology, which is the study of the aging process itself.

Ageing is a slow process that refers to the impact of passage of time on structure and function of different systems of body.

“Geriatrics” is cognate with Jara in Sanskrit which also means old.

JARA – OLD  AGE 

From

-              60 Years  (Charaka )

-              70 Years (Sushruta)

-              65 Years (W.H.O.)

Maximum Life Span Period  

-              100 years Ayurvedic and contemporary ancient Indian literature

-              125 years (Modern Science)

AYU  V/S  VAYA :

-              Ayu                        –              Chronological  Age

-              Vaya                      –              Biological   Age

 

SYNONYMS

  • JAYAS (That Which Has Grown)
  •  VARSHIAS (Fully Evolved Or Matured)
  •  JYESHATHA (That Which Is Older In Age)
  •  VARISHTH (That which is many years old)
  •  Other Synonyms Used For Old Age Are:

JARAN, JARATI, JARAUT, BRIDH

  •  Old Age Female are also referred as :

   NISHAPHALA, GATAARTAVA, PILANKANI,   SENESCENCE

 


Demographic Trends

l  World population of the elderly is increasing and by the year 2050, adult older than 65years will comprise 1/5th of the global population.

l  In India 3.8% population are older than 65 years of age.

l  It is estimated that the likely number of old age people in India by 2016 will be around 113 million

 

Ageing  A Continuous  Process

Acharya Sharangdhara described decade wise ageing.

 

INDICATED RASAYAN
1 Balyam Childhood Vacha, Swarna
2 Vriddhi Growth & Development Kashmari, Bala
3 Chhavi Lusture/Complexion Amalaki, Lauha
4 Medha Sharpeness in  perception Shankhapushpi
5 Twak Skin &  Appendages Bhringraj, Jyotismati
6 Drishti Visual Acuity Trifala, Shatavari
7 Shukra Potency & Fertility Atmagupta, Ashwagandha
8 Vikram Valor Amalaki, Bala
9 Buddhi Cummulative, Intellect & Cognitive functioning Brahmi
10 Karmindriya Physical capacities Bala, Ashwagandha

 

l  Finally there is loss of ultimate i.e. functions of mind and life substance.

l  The process of ageing begins the day  we are born or even conceived  and continues till death

-“Womb to Tomb” concept of ageing.

JARA HETU

l  Kalasya parinam – Swabhawaja Or Essential By Charak

l  Other Ayurvedic Literature Mentions Few Specific Hetu For Jara Especially  Aakal-Jara

l  Pantha – Excessive Travelling Or Physical Activities

l  Sheetam – Taking Unwholesome Or Chilled Food

l  Having Sexual Desires For Olderwomen Or To Remain Sexually Active Even After Onset Of Old-age.

l  Kaddana : Taking Tubers In Excess In Food.

l  Manaspratikoolta; To Remain Under Continuous mental stress.

Overindulgence of Gramyahara

l  Factor related to diet and dietetic habits

l  Factor related to daily routine activities

l  Factor related to psyche and personality

Provocation of Vata Dosha

l  Sithali bhawanti Mamsani

l  Vimunchyate Sandhya

l  Vishandate cha na alpameda

l  Shukram na pravartate

l  Kshyam-upait-oja

Features of Jara

l  Glayti (Physical and mental exertion)

l  Sidati (Muscular laxity of the body)

l  Nidratandralasya samanvita (Excess sleepiness, drowsiness and laziness)

l  Nirutsaha (Loss of enthusiasm)

l  Swasiti (Breathlessness)

l  Asamartha chestanam sharir- manasinam (Deterioration of  physical and mental activity)

l  Nashta smriti budhichaya (Loss of  memory, intellect and lusture of the body)

l  Roganam adhisthanabhuta (Becomes seat of diseases)

l  Nasaravamayu (Incomplete lifespan)

l  Sharirshaktiheena- Regression Of Physical Capacities

l  Smiritinasha – Diminishing Memory

l  Manasik Glani – Loss Of Cheerfulness And Alertness

l  Valinam – Appearance Of Wrinkles

l  Palitya – Greying Of Hair

l  Dantashaithilya – Loosening Of Denture

l  Swabhava  Vipparya – Change In Personality Components.

l  Kasa Swasa Pravritti – Proneness To Repeated Coughs And Dyspnoea On Effort

l  Sarvakriya Asamarthata ; Loss Of Physical, Perceptual And Mental Faculties

FEATURES OF VATAVRIDDHI IN OLD AGE

 

l  -KAYAPARUSHTA

l  -KARSHYA

l  -GATRASFURANA

l  -NIDRANASHA

l  -ALPABALATVAM

FEATURES OF DOSHA, DHATU AND MALA KSHAYA IN OLD AGE

l  Mandachesta – Slowness Of Physical And Mental Activities

l  Aapraharsh – Unsatisfying Nature

l  Mudhasangyata – Slowness Of Perception And Resolution

l  Nishprabhava – Loss Of Lusture

l  Rukshata – Dryness And Wasting

l  Sandhisaithilya – Unstability Of Joints

l  Manoshunyata – Lack Of Ideation

l  Shramm – Easy Fatigability

l  Shirashaithilya – Prominant And Tortuous Blood Vessels

l  Sfeek, Greeva, Udar Shuskata : Wasting Of Muscles

l  Asthi Shool – Degenerative Bone Disease

l  Klaibya – Erectile Dysfunctions And Sterility

FEATURES OF OJA KSHAYA IN OLD AGE

l  Durbalata- General debility

l  Rukshata – Dryness Of Skin

l  Vyathitendriya – Ailments And Diminished Capacities Of Indriyas.

l  Duschaya – Lack Of Lusture

l  Durmana – Decreased Mental Capacities

 

Examination plays an important role in older people since findings which are abnormal in the younger people are relatively common in the aged person.

Thus CROWN TO HEEL Examination Is Very Important

 

1)  Face  & Full  Body Posture –

            Should be noted to rule out CVA, TIA; since with age tendency of atherosclerosis, hypertension etc. increases which can lead to above problems.

2)  Eyes –

                           Blurred vision,

                           Blindness

                           Lens opacification

3)  Ears –

                           Difficulty discriminating words

                           High frequency activity

                           Thus bone conduction, Air conduction should be noted

 

4)  Dentures –

● True Or False

● If True –  The condition, strength, activity noted.

● If False – The proper denture set may be given.

5)  Respiratiory System –

● With age decrease lung elasticity and increase chest wall stiffness is seen leading to ventilation / perfusion mismatch and ↓ PO2 leading to Dyspnea; hypoxia.

6)  Breast-

● Older women are more likely to have breast cancer.

● Thus breast examination is important which may be overlooked by an old lady.

7)         Cardiovascular System :

● Decrease ß-adrenergic responsiveness – Decrease cardiac output and heart rate response to stress → heart failure.

● Systolic murmur of aortic sclerosis is common.

● 4th heart sound in elderly does not imply significant cardiac disease.

● Peripheral pulse – to rule out peripheral vascular disease, coarctation of aorta etc.

● B.P. with Postural (on sitting and standing) – to rule out postural hypotension.

8.) Gastro intestinal system :

● Decrease hepatic function               –           Cirrhosis

● Decrease Gastric acidity                   –           B12 deficiency, Iron deficiency, Anemia

● Decrease Colon motility                   –           Fecal impaction.

● Decrease Anorectal function          –           Fecal incontinence

● Organomegally should be noted

● Prolapse of rectum should be noted

9) Renal System

● Increase frequency  –                        Diabetes Mellitus

Prostate Enlargement

Urinary tract infection

● Nephropathy is also important complication with ageing.

● Distended bladder is mainly to be looked upon and treated.

● Incontinence is to be noted which may be due to Diabetic, Detrusor overactivity etc.

10) Genito-Urinary System

● Vaginal / Urethral, Mucosal atrophy

● Senile Vaginitis – yellow white discharge

● Prolapse of Uterus, Urethra, bladder, Intestine due to weakness of muscle, less of oestrogen etc. is common.

● Dyspareunia (difficult coitus)

● Impotency/ Erectile dysfunction            Both should be ruled out as complication of Diabetes Mellitus. Depression or Neuropathy.

11) Musculo Skeleton System

● Joint movement → rule out O.A., R.A.

● Muscle strength → wasting should be noted.

● Bony growth → osteoarthritic changes should be noted.

● Tenderness at Intervertebral disc is as important

12) Nervous System

● Reflexes – hyper/hypo – rule out upper / lower motor neuron deformity.

● Stiffer gait – Indicating Parkinsonism due to decreased dopaminergic synthesis.

● Rombergs sign – to rule out peripheral / central sensory deficit.

13) Endocrine System

● Impaired Glucose tolerance – Diabetes Mellitus

● ↓ Thyroxine – Thyroid Dysfunction

● ↓ Vitamin D absorption – Osteomalacia, Fracture

● ↓ Testosterone – Impotence

14) Mental Status

● Mild degree of Dementia, usually retain their social graces and may mask intellectual impairment by cheerful manner.

● Cognitive status i.e. identifying of person, object, self.

● Early awakening, sleep apnea

● Tension or continuous thinking or solved / unsolved topics.

● delirium etc are to be noted

Treatment

ADRAVYA CHIKITSA

l  CARE, ATENTION, LOVE can solve nearly 50% of geriatrics problems

l  It is the mental instability which is one of the important cause of Ageing Disease.

l  If a careful attention, love is given, and if we are able to remove the loneliness in life we can treat major problems.

l  Depression, confusion state, sleep apnea, early awakening, can be treated with care.

l  Careful listening to his problems, stories,

l  Serving him, entertaining him / her

l  Keeping them busy in things which are interesting for them and which are helpful.

Dravyabhuta (MEDICAL)

l  Samshodhan is mandatory before Rasayan therapy but in aged person Vaman, Virechan are contraindicated.

l  Mrudu Virechan with help of aragwada, draksha is helpfull

l  Acharyas believe that if panchakarma is essential mrudu samshodhan is indicated specially mrudu basti

l  Our Acharya have listed the rasayan kalpa for increasing good and healthy life span.

l  Medicine which will improve the activity of organ as well as do the nutrition of the organ.

l  Amalaki shatavari  etc are the ones which prevent free radical formation (Aam) act as antioxidant and increase life span

Rasayana Therapy (Rejuvenation)

l  Method to control / slow down /arrest the ageing process in human being.

l  Unique because of its ability to promote longevity and influence all expect of health.

l  Main utility in functional and degenerative disorders that have chronic or long standing nature.

Ashwagandha (Withania somnifera) used as herbal adaptogen containing. Withanotides and other alkaloids which stimulate the immune system.

Guduchi (Tinospora cordifolia) a rich source of natural vitamin C that has been proved to be effective in inhibiting the growth of bacteria and in building up the immune resistance, it also increases the killing ability of macrophages

Gokshura (Tribulus terrestris) contains saponins that may improve the heart function by dilating coronary arteries, thereby boosting circulation to heart

Arjuna (Terminalia arjuna) increases HDL to total cholesterol ratio and an overall improvement in cardiovascular profile

Haritaki (Terminalia chebula) a very rich content of Vitamin C and has strong anti-mutagenic activity.

Kapikacchu (Mucuna pruriens) a good natural source of L. Dopa  maintains optimum performance of nervous system

Kakamachi (Solanum nigrum) suppresses the oxidative degradation of DNA and therefore has a hepatoprotective

effect.

Kasani (Cichorium intybus) has a inhibitory effect on free radical induced DNA damage.

Kumkuma (Crocus sativus) contains number of carotenoid pigments generally known for their antioxidant properties. It is also a natural source for Riboflavin and Thiamine.

Guggulu (Commiphora mukul) increases WBC count and has a strong immuno-modulating properties.

Garcinia (Garcinia cambola) contains biologically active compounds Hydroxy Citric Acid which inhibits synthesis of lipids and fatty acids. It contains significant amount of Vitamin C and used as heart tonic.

Yashtimadhu (Glycyrrhiza glabra) acts as anti mutagen preventing damage to genetic material that can eventually result in cancer.

Meshashringi (Gymnema sylvestre) increases insulin production, regeneration of pancreas cells and the site of insulin production.

l  Similarly herbs like Shatawari (Asparagus racemosus)

l  Vridha daraka             (Argyreia speciosa)

l  Nagarmusta    (Cyperus scariosus)

l  Shigru              (Moringa pterygosperma) contains pterygospermin an antibiotic like substance

l  Jatamansi                    (Nardostachys jatamansi)

l  Pippali             (Piper longum)

l  Sunthi              (Zingiber officinale)

l  Musali             (Asparagus adscendens)

l  Mandukaparni            (Centella asiatic)

l  Bhringaraj                   (Eclipla alba)

l  Ghrut, taila internal & external use is essential for the elderly people

l  In general vatadosha samanya upakrama should be followed which can reduce dhatukshaya janya vataprakopa

l  Shiroabhyanga & shirodhara are useful in mental stress.

l  Medicines reducing hypertension, atherosclerosis D.M etc. should be taken according to medical advice.

l  Dose of insulin or hypoglycaemic drug should be given depending on FBSL & PP BSL in Diabetic person since tendency of patient going in hypoglycaemic / non–ketotic hyperosmolar shock is more

l  Digoxin may induce depression with normal serum levels.

l  Sympathominetics may precipitate urinary retention

l  Iatrogenic drug reaction should be noted

l  Diet should include

l  Vegetables – they decrease inflammation

l  Cabbage. Cauliflower, Potatoes, Tomatoes, Asparagus which are Glutathione rich foods. In fact without glutathione, other antioxidants such as vitamins C & E cannot do their job and protect you adequately against disease.

l  Fish are the natural resource of omega – 3 fatty acids it helps to decrease inflammation.

l  Cod liver Oil in effective in treating arthritic joint pain and even slowing or reversing the destruction of joint cartilage

l  Omega 3 fatty acid is present in Mackerel, Salmon, Sardines, Tuna Whitefish.

l  Use of flaxseed oil in cooking is a good source of Omega 3 fatty acids.

l  Olive oil has high concentrations of unsaturated fatty acids which decreased inflammation.

l  Soya-bean decreases  pain, it has other great benefits including being dairy free, low in saturated fat and excellent meat substitutes. It decreases the rate of heart diseases, breast cancer, prostate cancer and osteoporosis.

l  Fruits such as Grapes, Oranges, Peaches watermelon are good source of glutathione.

l  Pineapple contains enzyme called bromelain which help reduce inflammation mainly related with osteoarthritis and rheumatoid arthritis

l  Flavonoid are a family of more than four thousand compounds that include polypherols and they give colour to fruits and vegetables. These nutrients are powerful antioxidants and may hold key to disease prevention.

l  Green tea, onions, apples, soy and grapes are rich source of flavonoid.

l  Milk must be the most important dietary content of adult.

l  1 cup (250 ml) of 2%-fat milk contains 285 mg of calcium, which represents 22% to 29% of the daily recommended intake (DRI) of calcium for an adult.

l  Depending on the age, milk contains 8 grams of protein, and a number of other nutrients (either naturally or through fortification) including:

l  Biotin, Pantothenic acid, Iodine, Potassium, Magnesium, Selenium

Thiamine,  Vitamin A, Vitamin B12, Riboflavin, Vitamins D, Vitamin K

l  Calcium from dairy products has a greater bioavailability than calcium from certain vegetables, such as spinach.

Medical research

l  Studies show possible links between low-fat milk consumption and reduced risk of arterial hypertension, coronary heart disease, colorectal cancer and obesity.

l   Overweight individuals who drink milk may benefit from decreased risk of insulin resistance and type 2 diabetes.

l   Milk is a source of Conjugated linoleic acid.

l  It appears to be effective at promoting muscle growth

Treatment & Prevention are more effective for example

l  Benefits of treatment of Hypertension prevent chances of T.I.A.

l  Immunization against influenza & pneumococal pneumonia.

l  Increase bone calcium density to prevent fracture.

l  Improve balance, strength of legs, reduce peripheral oedema.

l  Eliminate environmental hazard, prevent accident

l  Replete nutritional deficit.

l  Prevent adverse modification which induce orthostatic, confusion, extrapyramidal stiffness

l  Give proper lens, improve vision.

l  Reduce extra physical mental stress

l  Give thrombolytic, ß-Blocker to prevent thrombus etc.

l  Endocrine supplement like thyroxine, oestrogen etc.

l  ↑ Calcium Supplement and other nutritional component

l  Counseling is important

LOVE THEM AND LET THEM LIVE LONG AND HEALTHY LIFE.

Geriatric nursing

Geriatric nursing is the specialty that concerns itself with the provision of nursing services to geriatric or aged individuals.

Geriatric nursing

l  . Due to their complexity, aged people always deserve personal attention.

l   Nurses address physical, psycho social, cultural and family concerns as well as promoting health and emphasizing successful aging.

l  Life expectancy is rising at rates which call for the proper preparation of nurses to take good care of the rapidly increasing number of the aged.

l  . Geriatric medications need to be managed so as to avoid too much use of medicine since this group receives a lot of medication if poor care is taken.

l  Multiple medications can cause a variety of drug interaction in older people.

Pressure injuries

l  A pressure ulcer is a lesion caused by unrelieved external pressure resulting from occlusion of the blood flow, tissue ischemia and cell death.

l   Pressure ulcers are often viewed as a complication of an acute or chronic illness.

l  The older people have an aged skin and due to exposure to the sun the skin wrinkles, epidermis thins, blood vessels recede, dermal-epidermal ridges flatten and the skin appears thin and fragile.

l  . When treating an ulcer wound treatment should focus on wound healing.

l  For a chronic, non healing ulcer, comfort should be a top priority.

l  For pressure injury careful positioning padding to reduce the risk of pressure ulceration is critical..

Cardiovascular disease

l  Cardiovascular disease is common in 50% of the population over the age of 65, and accounts for 40% of deaths in this group

l   When diagnosing look out for cases of fainting, continuous chest pain, nausea, shortness of breath, rapid heart rate, rapid weight gain, pain in the abdomen, swelling of legs among others. Then address the issue of hypertension, high blood cholesterol, diabetes, obesity and overweight, smoking, hereditary issues.

l  Treatment includes medication and physical exercises.

Respiratory issues

l  Nurse should draw a plan for treatment which includes working with other specialties like heart experts.

Genitourinary issues

l  Nurses should be careful with the language while carrying diagnosis so they can obtain as much information as possible.

Diabetes melitus

l  Nurse should emphasize nutrition and exercise which are vital for victims.

l   For older people monitoring for complications which can lead to lower extremity amputation, hypertension, myocardial infarction, stroke, vision loss, or nephropathy should be carried out especially in type 2 diabetic patient.

Thyroid

l  . Nurse Practioneers have a responsibility to evaluate and manage thyroid disorders by applying strategies specific to older adults.

Ethical and medico-legal issues

l  Elder abuse. Elder abuse is a general term used to describe certain types of harm to older adults

l  Power of attorney (endurable & durable). A power of attorney (POA) or letter of attorney in common law systems or mandate in civil law systems is an authorization to act on someone else’s behalf in a legal or business matter

l  End of life issues & Do Not Resuscitate (DNR) orders.

l  Euthanasia. Euthanasia (from the Greek meaning “good death”: ευ-, eu- (well or good) + thanatos (death)) refers to the practice of ending a life in a painless manner

DISORDERS OF THYROID AND PARATHYROID GLAND AND THEIR MANAGEMENT


PPT THYROID

Click link to download ppt  

DISORDERS OF THYROID AND PARATHYROID GLAND AND THEIR MANAGEMENT

by Prof. Dr. S. N. Ojha
  M.D. (Ayu.) Phd.
  Dean & Superintendent

  Dr. D. Y. Patil College of  Ayurveda & Research Centre
  Pimpri, Pune.
 
 

What is Thyroid?

Thyroid_gland

Thyroid

The thyroid is a small gland, shaped like a butterfly, located in the lower part of your neck. The main hormones released by the thyroid are triiodothyronine, (T3) & thyroxine, (T4)

What Diseases and Conditions Affect the Thyroid?

Hypothyroidism – An underactive thyroid.

Hyperthyroidism – an overactive thyroid.

Goiter – An enlarged thyroid.

Thyroid Nodules – Lumps in the thyroid gland.

Thyroid Cancer – Malignant thyroid nodules or tissue.

Thyroiditis – Inflammation of the thyroid.

Hyperthyroidism :

Hyperthyroidism is a condition where the thyroid gland – the master gland of metabolism – is overactive.

Causes of Hyperthyroidism

  1. Graves’ disease.
  2. Thyroiditis
  3. Autoimmune condition Hashimoto’s disease, a temporary hyperthyroidism that affects women

Risk of Graves’ Disease / Hyperthyroidism

  • Female gender
  • Personal and family history of thyroid problems, autoimmune disease, or endocrine disease
  • Age 20 and 40
  • Pregnancy – During pregnancy and the year after childbirth
  • Current or former smoker
  • Excessive intake of thyroid hormone
  • Exposure to or excess of iodine/iodine drugs
  • Certain medical treatments
  • Trauma to the thyroid
  • Recently experienced major life stress
  • Holistic and nutritional factors

Common symptoms

  • Goiter, thyroid enlargement, neck sensations
  • Weight and appetite changes
  • Pregnancy-related problems
  • Feeling warm all the time, sweating, thirst, fever
  • Heart and blood pressure changes, fast heart rate, abnormal heart rhythms
  • Bowel problems, diarrhea
  • Fatigue, exhaustion
  • Muscle and join pain and fatigue
  • Skin changes, blister-like bumps on the forehead and face, hives, itching, vitiligo.
  • Skin patches on the shins and legs (Graves’ dermopathy / pretibial myxedema)
  • Hair loss and other hair changes.
  • Finger/nail changes, including swollen, wider fingertips and separation of nail bed from skin.
  • Eye problems, including bulging, dryness, pain, redness, puffiness
  • Thinking/cognition problems, including difficult concentrating or making decisions, memory problems, and racing thoughts.
  • Changes to mood and feelings, including depression, mood swings, uncontrollable anger, irrational anger.
  • Panic and anxiety, panic attacks
  • Fast reflexes, startling, tremors
  • Insomnia

Diagnosing Graves’ Disease

Clinical Exam.

  • Feel (also known as “palpating”) neck
  • Palpate for what’s known as “thrill”
  • Listen for “bruit” during palpation
  • Test reflexes-hyper responsive reflexes can be a sign of hyperthyroidism
  • Heart rate, rhythm & blood pressure
  • Measure weight
  • Measure body temperature
  • Examine face and neck area
  • Examine skin for some possible signs of hyperthyroidism
  • General quantity and quality of hair
  • Tremors
  • Nails and hands for thyroid signs
  • Evaluate legs
  • Examine eyes

Test results that confirm hyperthyroidism include:

  • TSH Test – usually below normal, to undetectable
  • T4/Free T4 Test – Normal to High
  • T3/Free T3 Test – Normal to High

Radioactive Iodine Update (RAI-U) Test

  • Elevated Thyroid Receptor Antibodies (TRAb) /
  • Thyroid-Stimulating Immunoglobulin (TSI).

Hyperthyroidism – can be treated with three different approaches:

  • Drug treatment with antithyroid drugs
  • Ablation of the thyroid gland with Radioactive Iodine (RAI)
  • Surgery to remove all or part of the thyroid.

Antithyroid Drug Treatment

  • Methimazole – Carbimazole
  • Propylthiouracil

Radioactive Iodine Treatment

-          Radioiodine ablation

-          Radioactive iodine ablation

-          Thyroid ablation

-          Ablation therapy

-          Chemical thyroidectomy

-          Chemical surgery

-          Radioactive cocktail

Ayurvedic Treatment

  • Kanchanar Guggulu
  • Aarogyavardhini Rasa
  • Sootshekhar Rasa
  • Dasha moolarishta

Hypothyroidism :

When the thyroid gland is underactive, improperly formed at birth, surgically removed all or in part, or becomes incapable of producing enough thyroid hormone, a person is said to the hypothyroid.

Causes

  • Iodine deficiency
  • Hashimoto’s thyroiditis
  • Lack of the thyroid gland
  • Deficiency of hormones from either the hypothalamus or the pituitary.
  • Postpartum thyroiditis
  • Sporadic inheritance, sometimes autosomal recessive
  • Wolff-Chaikoff effect
  • Lithium-based mood stabilizers

Symptoms

Early symptoms

  • Poor muscle tone
  • Fatigue
  • Cold intolerance
  • Depression
  • Muscle cramps and joint pain
  • Arthritis
  • Goiter
  • Thin, brittle fingernails
  • Thin, brittle hair
  • Paleness
  • Dry, itchy skin
  • Weight gain and water retention
  • Bradycardia (low heart rate: less than sixty beats per minute)
  • Constipation

Late symptoms

  • Slow speech and a hoarse, breaking voice.
  • Dry puffy skin, especially on the face
  • Thinning of the outer third of the eyebrows. (sign of Hertoghe)
  • Abnormal menstrual cycles
  • Low basal body temperature

Less common symptoms

  • Migraine headache
  • Impaired memory
  • Anxiety / panic attacks
  • Urticaria
  • Impaired cognitive function and inattentiveness
  • A slow heart rate with ECG changes including low voltage signals.
  • Reactive (or post-prandial) hypoglycemia
  • Pericardial effusions may occur.
  • Sluggish reflexes
  • Hair loss
  • Early greying of the hair
  • Anemia caused by impaired hemoglobin synthesis
  • Difficulty swallowing
  • Shortness of breath with a shallow and slow respiratory pattern
  • Hypercapnia & hypoxia
  • Increased sleep
  • Osteopenia or Osteoporosis
  • Irritability and mood instability
  • Yellowing of the skin
  • Impaired renal function
  • Thin, fragile or absent cuticles
  • Elevated serum cholesterol
  • Acute psychosis
  • Decreased libido
  • Decreased sense of taste and smell
  • Puffy face, hands and feet
  • Premature wrinkling on the face

Pediatric

  • Short stature
  • Mental retardation
  • Short neck
  • Delayed development

Severity

  • Cardiovascular & psychiatric
  • Myxedema

Diagnostic testing

  • Free triiodothyronine (fT3)
  • Free levothyroxine (fT4)
  • Total T3
  • Total T4
  • 24 hour urine free T3
  • antithyroid antibodies
  • Serum cholesterol
  • Prolactin
  • Testing for anemia, including ferritin
  • Basal body temperature

Treatment

  • Levorotatory forms of thyroxin (L-T4)
  • Different treatment protocols in thyroid replacement therapy:
  • T4 Only
  • T4 and T3 in Combination
  • Desiccated Thyroid Extract

Ayurvedic Treatment

  • Laxmivilas Rasa
  • Punarnavadi Mandur
  • Agnitundi Vati
  • Ashwagandharishta
  • Amrtarishta
  • Shatavari
  • Chitrak
  • Chatusparni

Autoimmune Thyroid Disease

In the case of autoimune thyroid disease, antibodies either gradually destroy the thyroid, or make it overactive.

  • Goiter/Thyroid Nodules

When the thyroid become enlarged, this is known as a goiter.

  • Thyroid Cancer
  • Thyroiditis

When the thyroid become inflamed, due to bacterial or viral illness, this is known as thyroiditis

Treatments – Surgery, Thyroid drugs

Parathyroid gland

  • The parathyroid glands are small endocrine gland in the neck that produces parathyroid hormone.
  • Most people have four parathyroid glands, but some people have six or even eight

Hypoparathyroidism

  • It is decreased function of parathyroid glands, leading to decreased levels of parathyroid hormone (PTH).

Causes

  • Removal of the parathyroid glands in thyroid surgery (thyroidectomy)
  • Autoimmune.
  • Hemochromatosis
  • Chromosome 22q11 microdeletion syndrome (other names: DiGeorge syndrome Schprintzen syndrome, velocardiofacial syndrome).
  • Magnesium deficiency
  • DiGeorge syndrome, absence of the parathyroid glands at birth.
  • Idiopathic, occasionally familial

Signs and Symptoms

  • Tingling lips, fingers, and toes
  • Muscle cramps
  • Pain in the face, legs, and feet
  • Abdominal pain
  • Dry hair
  • Brittle nails
  • Dry, scaly skin
  • Cataracts
  • Weakened tooth enamel (in children)
  • Muscle spasms called tetany
  • Convulsions (seizures)

Additional symptoms

  • Painful menstruation
  • Hand or foot spasms
  • Decreased consciousness
  • Delayed or absent tooth formation

Diagnosis

  1. Measurement of calcium
  2. Serum albumin
  3. PTH in blood.
  4. E.C.G.

Differential diagnoses are:

  • Pseudohypoparathyroidism
  • Pseudopseudohypoparathyroidism
  • Vitamin D deficiency or hereditary insensitivity to this vitamin (X-linked dominant).
  • Malabsorption
  • Kidney disease
  • Medication: Steroids, diuretics, some antiepileptics.

Treatment

1.            Intravenous calcium

Long-term treatment

  • Calcium and Vitamin D 3
  • Teriparatide

Possible Complications

  • Tetany can lead to a blocked airway
  • Stunted growth, malformed teeth, slow mental development
  • Overtreatment with vitamin D and calcium can cause hypercalcemia

 

Pseudohypoparathyroidism

  • Pseudohypoparathyroidism is a condition caused by resistance to the parathyroid hormone.
  • Patients have a low serum calcium and high phosphate, but the parathyroid hormone level (PTH) is appropriately high.

Types

  • Type 1 a pseudohypoparathyroidism
  • Type 1 b pseudohypoparathyroidism lacks the physical appearance of type 1 a biochemically similar
  • Type 2 pseudohypoparathyroidism also lacks the physical appearance of type 1 a.

Presentation

  • Features of hypocalcaemia
  • Including; carpo-pedal spasm, tetany, muscle cramps and seizures.
  • Type 1 a Pseudohypoparathyroidism is clinically manifest by blunting of fourth and fifth                 metacarpals, short stature, obesity, developmental delay.

Biochemical Findings

  • Hypocalcemia
  • Hyperphosphatemia
  • Elevated parathyroid hormone

Hypocalcemia

  • Muscle spasm
  • Carpopedal spasm
  • facial grimacing
  • Layrngeal spasm
  • Convulsion
  • Respiratory arrest may occur
  • Increase intracranial pressure
  • Irritability
  • Depression
  • Psychosis
  • Arrhythmias
  • Intestinal cramps
  • Chvostek’s or Trousseaus Sign

Treatment

  • Replacement with Vit. D or Calcitriol
  • High oral calcium intake
  • Thiazide diuretics

Ayurvedic Treatment

  • Godanti
  • Praval Panchamruta

Hyperparathyroidism

Hyperparathyroidism is overactivity of the parathyroid glands resulting in excess production of parathyroid hormone (PTH)

Classification

Primary Hyperparathyroidism

It results from a hyper function of the parathyroid glands themselves. There is over secretion of PTH due to adenoma, hyperplasia or rarely, carcinoma of the parathyroid glands.

Secondary hyperparathyroidism

Secondary hyperparathyroidism is the reaction of the parathyroid glands to a hypocalcemia caused by something other than a parathyroid pathology, e.g. chronic renal failure.

Tertiary Hyperparathyroidism

Tertiary hyperparathyroidism is a state of excessive secretion of parathyroid hormone (PTH) after a long period of secondary hyperparathyroidism and resulting in hypercalcemia.

Etiology

Primary hyperparathyroidism

1. benign parathyroid adenoma

2. multiple endocrine neoplasia

Secondary hyperparathyroidism

Due to excessive secretion of parathyroid hormone (PTH) by parathyroid glands in response to hypocalcemia and/or hyperphosphatemia, usually due to chronic renal failure.

Tertiary hyperparathyroidism

Caused by long lasting disorders of the calcium feedback control system.

Symptoms and signs

Asymptomatic hyperparathyroidism

Coincidental finding of hypercalcemia

Symptomatic Hyperparathyroidism

Most of the symptoms of parathyroid disease are “neurological”

weakness and fatigue,

depression,

aches and pains,

decreased appetite,

feelings of nausea and vomiting,

constipation,

polyuria,

polydipsia,

cognitive impairment,

kidney stones and

osteoporosis.

Symptoms of hyperparathyroidism can be remembered by the rhyme “moans, groans, stones, bones, and psychiatric overtones” :

  • “moans” (complaints of not feeling well)
  • “groans” (abdominal pain, gastroesophageal reflux)
  • “stones” (kidney)
  • “bones” (bone pain)
  • “psychiatric overtones” (lethargy, fatigue, depression, memory problems

Laboratory tests

Serum calcium

  • In cases of primary, tertiary hyperparathyroidism             increased PTH consequently leads to increased                 serum calcium (hypercalcemia)
  • In secondary hyperparathyroidism effectiveness              of PTH is reduced.

Serum phosphorus

  • Primary hyperparathyroidism levels are                abnormally low
  • Secondary hyperparathyroidism serum                 phosphorus levels are generally elevated
  • Alkaline phosphatase
  • Alkaline phosphatese levels are not elevated in all types of hyperparathyroidism

Diagnosis

  • PTH immunoassay
  •   Tertiary hyperparathyroidism has a high PTH and high serum

calcium.

Treatment and monitoring

  • Surgery

If surgery is not available, the following should be monitored

  • Calcium level
  • Bone density
  • Check for kidney stones

Prevention

  • Exercise
  • Vitamin D-Adequate amounts of vitamin D aid in calcium absorption.
  • Stay hydrated
  • No smoking

Hypercalcemia

  • Fatigue
  • Depression
  • Mental Confusion
  • Anorexia
  • Nausea
  • Vomiting
  • Constipation
  • Increased urination
  • Cardiac arrythmias

Treatment

  • Restricted Dietary Calcium
  • Rehydration
  • Forced Diuresis
  • Calcitonin
  • Anti resorptive agents (bisphosphonates)
  • Phosphate therapy

How Do you rate this site!
(polls)


Understanding Hypertension.


Hypertension


Hypertension can be classified as either essential (primary) or secondary.

high blood presure

Hypertension is a chronic medical condition in which the blood pressure is elevated.

 It is also referred to as high blood pressure or shortened to HT, HTN or HPN.

 The word “hypertension”, by itself, normally refers to systemic, arterial hypertension.

Essential or primary hypertension means that no medical cause can be found to explain the raised blood pressure. It is common. About 90-95% of hypertension is essential hypertension.

Secondary hypertension indicates that the high blood pressure is a result of (i.e., secondary to) another condition, such as kidney disease or tumours (adrenal adenoma or pheochromocytoma).

Persistent hypertension is one of the risk factors for strokes, heart attacks, heart failure and arterial aneurysm, and is a leading cause of chronic renal failure.

Even moderate elevation of arterial blood pressure leads to shortened life expectancy.

 Classification

Classification

Systolic pressure

Diastolic pressure

mmHg

kPa

mmHg

kPa

Normal 90–119 12–15.9 60–79 8.0–10.5
Prehypertension 120–139 16.0–18.5 80–89 10.7–11.9
Stage 1 140–159 18.7–21.2 90–99 12.0–13.2
Stage 2 ≥160 ≥21.3 ≥100 ≥13.3
Isolated systolic
hypertension
≥140 ≥18.7 <90 <12.0
Source: American Heart Association (2003).

Resistant hypertension is defined as the failure to reduce blood pressure to the appropriate level after taking a three-drug regimen (include thiazide diuretic).

 Excessive elevation in blood pressure during exercise is called exercise hypertension.

Exercise hypertension may be regarded as a precursor to established hypertension at rest.

Signs and symptoms

Mild to moderate essential hypertension is usually asymptomatic

 Accelerated hypertension is associated with

            headache,   somnolence, confusion, visual disturbances,  nausea and vomiting (hypertensive encephalopathy).

Retinas are affected with narrowing of arterial diameter to less than 50% of venous diameter, copper or silver wire appearance, exudates, hemorrhages, or papilledema.

Some signs and symptoms are especially important in infants and neonates such as

 failure to thrive, seizure, irritability, lethargy, and respiratory distress.

While in childrens hypertension may cause headache,  fatigue, blurred vision, epistaxis, and bell palsy.


signs and symptoms are especially important in suggesting a secondary medical cause of chronic hypertension, such as centripetal obesity, “buffalo hump,”  and/or wide purple abdominal striae and maybe a recent onset of diabetes suggest glucocorticoid excess either due to Cushing’s syndrome or other causes.

Hypertension due to other secondary endocrine diseases such as hyperthyroidism, hypothyroidism, or growth hormone excess show symptoms specific to these disease such as

in hyperthyrodism there may be

weight loss, tremor, tachycardia or atrial arrhythmia, palmar erythema and sweating.

Signs and symptoms associated with growth hormone excess

such as coarsening of facial features, prognathism, macroglossia,  hypertrichosis, hyperpigmentation, and hyperhidrosis.

hyperaldosteronism may cause less specific symptoms such as

 numbness,  polyuria,  polydipsia, hypernatraemia, and metabolic alkalosis.

 A systolic bruit heard over the abdomen or in the flanks suggests renal artery stenosis.

Also radio femoral delay or diminished pulses in lower versus upper extremities suggests coarctation of the aorta.

 Hypertension in patients with pheochromocytomas is usually sustained but may be episodic.

 The typical attack lasts from minutes to hours and is associated with

headache, anxiety, palpitation, profuse perspiration, pallor, tremor, and nausea and vomiting.

 Blood pressure is markedly elevated, and angina or acute pulmonary edema may occur.

In primary aldosteronism, patients may have

muscular weakness,  polyuria, and nocturia due to hypokalemia.

 Chronic hypertension often leads to left ventricular hypertrophy, which can present with exertional and paroxysmal nocturnal dyspnea.

 Cerebral involvement causes stroke due to thrombosis or hemorrhage from microaneurysms of small penetrating intracranial arteries.

 Hypertensive encephalopathy is probably caused by acute capillary congestion and exudation with cerebral edema, which is reversible.

 Signs and symptoms associated with pre-eclampsia and eclampsia, can be

proteinuria, edema, and hallmark of eclampsia which is convulsions,

Other cerebral signs may precede the convulsion such as nausea, vomiting, headaches, and blindness.

Causes

Essential hypertension

By definition, has no identifiable cause.

 It is the more common type and affects 90-95% of hypertensive patients,

even though there are no direct causes, there are many risk factors such as

sedentary lifestyle, obesity (more than 85% of cases occur in those with a body mass index greater than 25), salt (sodium) sensitivity, alcohol intake, and vitamin D deficiency, aging, inherited genetic mutations.

 Family history increases the risk of developing hypertension.

 Renin elevation is another risk factor, Renin is an enzyme secreted by the juxtaglomerular apparatus of the kidney and linked with aldosterone in a negative feedback loop

 Also sympathetic overactivity is implicated.

 Insulin resistance which is a component of syndrome X, or the metabolic syndrome is also thought to cause hypertension.

 Recently low birth weight has been questioned as a risk factor for adult essential hypertension.

Secondary hypertension

Secondary hypertension by definition results from an identifiable cause

Many secondary causes can cause hypertension such as

Cushing’s syndrome, which is a condition where both adrenal glands can overproduce the hormone cortisol.

 Hypertension results from the interplay of several pathophysiological mechanisms regulating plasma volume, peripheral vascular resistance and cardiac output, all of which may be increased. More than 80% of patients with Cushing’s syndrome have hypertension.]

Another important cause is the congenital abnormality coarctation of the aorta.

Adrenal

In primary aldosteronism there is a clear relationship between the aldosterone-induced sodium retention and the hypertension.

 Another related disorder that causes hypertension is apparent mineralocorticoid excess syndrome which is an autosomal recessive disorder results from mutations in gene encoding 11β-hydroxysteroid dehydrogenase which normal patient inactivates circulating cortisol to the less-active metabolite cortisone.[60] Cortisol at high concentrations can cross-react and activate the mineralocorticoid receptor, leading to aldosterone-like effects in the kidney, causing hypertension.

Frequently, if liquorice is the cause of the high blood pressure, a low blood level of potassium will also be present.

 Yet another related disorder causing hypertension is glucocorticoid remediable aldosteronism, which is an autosomal dominant disorder in which the increase in aldosterone secretion produced by ACTH is no longer transient, causing of primary hyperaldosteronism, the Gene mutated will result in an aldosterone synthase that is ACTH-sensitive, which is normally not. GRA appears to be the most common monogenic form of human hypertension.

 Compare these effects to those seen in Conn’s disease, an adrenocortical tumor which causes excess release of aldosterone, that leads to hypertension.

Cushing’s syndrome which is a disorder caused by high levels of cortisol. Cortisol is a hormone secreted by the cortex of the adrenal glands

 Kidney

Polycystic kidney disease which is a cystic genetic disorder of the kidneys,

PKD is characterized by the presence of multiple cysts (hence, “polycystic”) in both kidneys, can also damage the liver, pancreas, and rarely, the heart and brain.

 It can be autosomal dominant or autosomal recessive, with the autosomal dominant form being more common and characterized by progressive cyst development and bilaterally enlarged kidneys with multiple cysts, with concurrent development of hypertension, renal insufficiency and renal pain

chronic glomerulonephritis which is a disease characterized by inflammation of the glomeruli, or small blood vessels in the kidneys.

 Hypertension can also be produced by diseases of the renal arteries supplying the kidney. This is known as renovascular hypertension; it is thought that decreased perfusion of renal tissue due to stenosis of a main or branch renal artery activates the renin-angiotensin system

 also some renal tumors can cause hypertension.

Juxtaglomerular cell tumor, Wilms’ tumor, and renal cell carcinoma, all of which may produce renin.

 Neuroendocrine tumors are also a well known cause of secondary hypertension.

Pheochromocytoma (most often located in the adrenal medulla) increases secretion of catecholamines such as epinephrine and norepinephrine, causing excessive stimulation of adrenergic receptors, which results in peripheral vasoconstriction and cardiac stimulation

Medication side effects

NSAIDs (Motrin/Ibuprofen) and

steroids can cause hypertension

 High blood pressure that is associated with the sudden withdrawal of various antihypertensive medications is called rebound hypertension., rebound hypertension may result in a hypertensive emergency.

Rebound hypertension is avoided by gradually reducing the dose (also known as “dose tapering”), thereby giving the body enough time to adjust to reduction in dose. Medications commonly associated with rebound hypertension include centrally-acting antihypertensive agents, such as clonidine and beta-blockers.

Pregnancy

Few women of childbearing age have high blood pressure, up to 11% develop hypertension of pregnancy.

, it may herald three complications of pregnancy:

pre-eclampsia,

HELLP syndrome and

eclampsia.

Sleep disturbances

sleep apnea

neurological disease called Binswanger’s disease, causing dementia; it is a rare form of multi-infarct dementia, and is one of the neurological syndromes associated with hypertension.

Pathophysiology

What is known is that cardiac output is raised early in the disease course, with total peripheral resistance (TPR) normal; over time cardiac output drops to normal levels but TPR is increased.

Three theories have been proposed to explain this:

  • Inability of the kidneys to excrete sodium, resulting in natriuretic factors such as Atrial Natriuretic Factor being secreted to promote salt excretion with the side effect of raising total peripheral resistance.
  • An overactive Renin-angiotensin system leads to vasoconstriction and retention of sodium and water. The increase in blood volume leads to hypertension.
  •  An overactive sympathetic nervous system, leading to increased stress responses.
  •  It is also known that hypertension is highly heritable and polygenic (caused by more than one gene) and a few candidate genes have been postulated in the etiology of this condition.

Diagnosis

complete history

physical examination to confirm a diagnosis of hypertension.

 Characteristically, a “hypertensive headache” occurs in the morning and is localized to the occipital region.

Other nonspecific symptoms that may be related to elevated blood pressure include dizziness, palpitations, easy fatiguability, and impotence.

Laboratory tests

Secondary hypertension is more common in preadolescent children, with most cases caused by renal disease.

 Primary or essential hypertension is more common in adolescents and has multiple risk factors, including obesity and a family history of hypertension.

Tests done are classified as follows:

System

Tests

Renal Microscopic urinalysis, proteinuria, serum BUN (blood urea nitrogen) and/or creatinine
Endocrine Serum sodium, potassium, calcium, TSH (thyroid-stimulating hormone).
Metabolic Fasting blood glucose, total cholesterol, HDL and LDL cholesterol, triglycerides
Other Hematocrit, electrocardiogram, and Chest X-ray

Creatinine (renal function) testing is done to identify both the underlying renal disease as a cause of hypertension and, conversely, hypertension causing the onset of kidney damage.

It is a baseline for monitoring the possible side-effects of certain antihypertensive drugs later.

Glucose testing is done to identify diabetes mellitus.

Additionally, testing of urine samples for proteinuria detection is used to pick up an underlying kidney disease or evidence of hypertensive renal damage.

Electrocardiogram (EKG/ECG) testing is done to check for evidence of the heart being under strain from working against a high blood pressure

A chest X-ray might be used to observe signs of cardiac enlargement or evidence of cardiac failure.

Prevention

The degree to which hypertension can be prevented depends on a number of features including: current blood pressure level, changes in end/target organs (retina, kidney, heart – among others), risk factors for cardiovascular diseases and the age at presentation.

  • Weight reduction and regular aerobic exercise (e.g., walking) are recommended as the first steps in treating mild to moderate hypertension. Regular exercise improves blood flow and helps to reduce resting heart rate and blood pressure.
  •  Reducing dietary sugar intake.
  • Reducing sodium (salt) in the diet may be effective: It decreases blood pressure in about 33% of people (see above
  • Diet which is rich in fruits and vegetables and low-fat or fat-free dairy foods
  •  In addition, an increase in daily calcium intake has the benefit of increasing dietary potassium, which theoretically can offset the effect of sodium and act on the kidney to decrease blood pressure.
  • Discontinuing tobacco use and alcohol consumption has been shown to lower blood pressure.
  • Reducing stress, for example with relaxation therapy, such as meditation and other mindbody relaxation techniques
  •  by reducing environmental stress such as high sound levels and over-illumination can be an additional method of ameliorating hypertension.
  • Jacobson’s Progressive Muscle Relaxation and biofeedback are also used,[  particularly, device-guided paced breathing, although meta-analysis suggests it is not effective unless combined with other relaxation techniques.
  • Treatment

Lifestyle modifications

Lifestyle changes such as the DASH diet,

 physical exercise,

 and weight loss have been shown to significantly reduced blood pressure in people with high blood pressure.

UK Hypertension guidelines

Thresholds for starting treatment

Group

Target of treatment

>160/100 all those with such persisting readings <140/90
>140/90 If also: Cardiovascular risk >20% per 10 years
Or have established cardiovascular disease
Or have evidence end organ damage
Or chronic kidney disease without high levels albuminuria
<140/90
>130/80 Type 2 Diabetes alone <130/80
>135/85 Type 1 Diabetes alone <130/80
>130/80 Type 1 Diabetes with microalbuminuria
Or Type 2 Diabetes with kidney, eye or cerebrovascular damage
<130/80
>130/80 chronic kidney disease with high levels albuminuria <125/75

Biofeedback

Biofeedback devices can be used alone or in conjunction with lifestyle changes or medications to monitor and possibly reduce hypertension. One example is Resperate, a portable, battery-operated personal therapeutic medical device, sold over the counter (OTC) in the United States. However, claims of efficacy are not supported by scientific studies. Testimonials are used to promote such products, while no real evidence exists that the use of resperate like devices lowers any morbidity associated with hypertension.

Medications

The aim of treatment should be blood pressure control to <140/90 mmHg for most patients, and lower in certain contexts such as diabetes or kidney disease (some medical professionals recommend keeping levels below 120/80 mmHg).

 Commonly used drugs include the typical groups of

            ACE inhibitors such as captopril, enalapril, fosinopril (Monopril), lisinopril (Zestril), quinapril, ramipril (Altace)

  • Angiotensin II receptor antagonists may be used where ACE inhibitors are not tolerated: eg, telmisartan (Micardis, Pritor), irbesartan (Avapro), losartan (Cozaar), valsartan (Diovan), candesartan (Amias), olmesartan (Benicar, Olmetec)
  • Calcium channel blockers such as nifedipine (Adalat) amlodipine (Norvasc), diltiazem, verapamil
  • Diuretics: eg, bendroflumethiazide, chlorthalidone, hydrochlorothiazide (also called HCTZ).

Other additionally used groups include:

  • Additional diuretics such a furosemide or low-dosages of spironolactone
  • Alpha blockers such as prazosin, or terazosin. Doxazosin has been shown to increase risk of heart failure, and to be less effective than a simple diuretic.
  • Beta blockers such as atenolol, labetalol, metoprolol (Lopressor, Toprol-XL), propranolol.
  • Direct renin inhibitors such as aliskiren (Tekturna).

Choice of initial medication

For mild blood pressure elevation,

 consensus guidelines call for medically-supervised lifestyle changes and observation before recommending initiation of drug therapy.

If lifestyle changes are ineffective, then drug therapy is initiated, often requiring more than one agent to effectively lower hypertension.

thiazide-type diuretics are better and cheaper than other major classes of drugs at preventing cardiovascular disease, and should be preferred as the starting drug.

Thiazide diuretics are effective

. Hydrochlorothiazide is perhaps the safest and most inexpensive agent

Doses in excess of 25 milligrams per day of this agent incur an unacceptable risk of low potassium or Hypokalemia.

 Patients with an exaggerated hypokalemic response to a low dose of a thiazide diuretic should be suspected to have Hyperaldosteronism, a common cause of secondary hypertension.

Adverse effects of thiazide diuretics include hypercholesterolemia,

 and impaired glucose tolerance with increased risk of developing Diabetes mellitus type 2.

The thiazide diuretics also deplete circulating potassium unless combined with a potassium-sparing diuretic or supplemental potassium.

Current UK guidelines suggest starting patients over the age of 55 years and all those of African/Afrocaribbean ethnicity firstly on calcium channel blockers or thiazide diuretics,

 whilst younger patients of other ethnic groups should be started on ACE-inhibitors.

Subsequently if dual therapy is required to use ACE-inhibitor in combination with either a calcium channel blocker or a (thiazide) diuretic.

 Triple therapy is then of all three groups and should the need arise then to add in a fourth agent, to consider either a further diuretic (e.g. spironolactone or furosemide), an alpha-blocker or a beta-blocker.

Prognosis

It is based upon several factors

including genetics

 dietary habits,

 and overall lifestyle choices

Complications

Hypertension is a risk factor for all clinical manifestations of atherosclerosis since it is a risk factor for atherosclerosis itself.

 It is an independent predisposing factor for heart failure, coronary artery disease, stroke, renal disease, and peripheral arterial disease.

 it is the most important risk factor for cardiovascular morbidity and mortality in industrialized countries.[176] The risk is increased for:

  • Cerebrovascular accident (CVAs or strokes)
  • Myocardial infarction (heart attack)
  •  Hypertensive cardiomyopathy (heart failure due to chronically high blood pressure)
  • Left ventricular hypertrophy – thickening of the myocardium (muscle) of the left ventricle of the heart.
  •  Hypertensive retinopathy – damage to the retina
  • Hypertensive nephropathy – chronic renal failure due to chronically high blood pressure “benign nephrosclerosis”.
  • Hypertensive encephalopathy – confusion, headahe, convulsion due to vasogenic edema in brain due to high blood pressure.

Epidemiology

It is estimated that nearly one billion people are affected by hypertension worldwide, and this figure is predicted to increase to 1.5 billion by 2025

Over 90-95% of adult hypertension is of the essential hypertension type.

being higher in blacks and lower in whites and Mexican Americans ;

second it changes with age,

; also geographic patterns, because hypertension is more prevalent in the southeastern United States;

 another important one is gender, because hypertension is more prevalent in men (though menopause tends to abolish this difference);

 and finally socioeconomic status, which is an indicator of lifestyle attributes and is inversely related to the prevalence, morbidity, and mortality rates of hypertension.

 For the secondary hypertension its known that primary aldosteronism is the most frequent endocrine form of secondary hypertension

The incidence of exercise hypertension is reported to range from 1 to 10% of the total population.

Hypertension often is part of the metabolic “syndrome X” its co-occurring with other components of the syndrome.

The other components are, diabetes mellitus, combined hyperlipidemia, and central obesity.

Children and adolescents

The epidemic of childhood obesity,

Renal parenchymal disease is the most common (60 to 70%) cause of hypertension.

 Adolescents usually have primary or essential hypertension, making up 85 to 95% of cases

. Medical students commonly suffer from hypertension especially mature students.

History

Some cite the writings of Sushruta in the 6th century BC as being the first mention of symptoms like those of hypertension.

Our modern understanding of hypertension began with the work of physician William Harvey (1578–1657).

It was then recognized as a disease a century later by Richard Bright (physician) in (1789–1858).

The first ever elevated blood pressure in a patient without kidney disease was reported by Frederick Mahomed (1849–1884).

  1. Hypertension (High Blood Pressure)

 Food/Diet Therapy for Hypertension

Vegetarian Diet

Vegetarians, in general, have lower blood pressure levels and a lower incidence of hypertension and other cardiovascular diseases. Experts postulate that a typical vegetarian’s diet contains more potassium, complex carbohydrates, polyunsaturated fat, fiber, calcium, magnesium, vitamin C and vitamin A, all of which may have a favorable influence on blood pressure.

Fiber

A high-fiber diet has been shown to be effective in preventing and treating many forms of cardiovascular disease, including hypertension.
The types of dietary fiber is important. Of the greatest benefit to hypertension are the water soluble gel-forming fibers such as oat bran, apple pectin, psyllium seeds, and guar gum. These fibers, in addition to be of benefit against hypertension, are also useful to reduce cholesterol levels, promote weight loss, chelate out heavy metals, etc.

  1. Sugar

Sucrose, common table sugar, elevates blood pressure. Underlying mechanism is not clearly understood. It is possible that sugar increases the production of adrenaline, which in turn, increases blood vessel constriction and sodium retention.

Reduce Salt and Sodium in Your Diet

A key to healthy eating is choosing foods lower in salt and sodium

Excessive consumption of dietary sodium chloride (salt), coupled with diminished dietary potassium, induces an increase in fluid volume and an impairment of blood pressure regulating mechanisms. This results in hypertension in susceptible individuals.

A high potassium-low sodium diet reduces the rise in blood pressure during mental stress by reducing the blood vessel constricting effect of adrenaline. Sodium restriction alone does not improve blood pressure control; it must be accompanied by a high potassium intake.

Beneficial Vegetables and Spices for Hypertension

Celery (Apium graveolens). Oriental Medicine practitioners have long used celery for lowering high blood pressure.

Garlic (Allium sativum). Garlic is a wonder drug for heart. It has beneficial effects in all cardiovascular system including blood pressure.

Onion (Allium cepa). Onions are useful in hypertension. What is best is the onion essential oil. Two to three tablespoons of onion essential oil a day was found to lower the systolic levels by an average of 25 points and the diastolic levels by 15 points in hypertension subjects.

Tomato (Lycopersicon lycopersicum). Tomatoes are high in gamma-amino butyric acid (GABA), a compound that can help bring down blood pressure.

Broccoli (Brassica oleracea). This vegetable contains several active ingredients that reduce blood pressure.

Carrot (Daucus carota). Carrots also contain several compounds that lower blood pressure.

Saffron (Crocus sativus).

Saffron contains a chemical called crocetin that lowers the blood pressure.

Assorted spices

Spices such as fennel, oregano, black pepper, basil and tarragon have active ingredients that is beneficial in hypertension

MODERN & AYURVEDA PERSPECTIVE OF SICKLE CELL ANAEMIA


Prof. Dr. S. N. Ohja

 

 

 

 

MODERN & AYURVEDA PERSPECTIVE OF SICKLE CELL ANAEMIA

Prof. S . N. Ojha (M.D.(Ayu.) Ph.D.)

Principal,

Pad. Dr. D. Y. Patil College of Ayurved  & Research Centre, Pimpri, Pune


Introduction

Sickle cell disease, or sickle – cell anaemia (or  drepanocytosis), is a genetic life-long blood disorder characterized by RBC that assume an abnormal, rigid, sickle shape.  Sickling decreases the cells flexibility and results in a risk of various complications. Life expectancy is shortened, average life expectancy of 42, & 48 years for males & females respectively.

Prevalence

Sickle cell disease, occurs more commonly in people from parts of tropical & subtropical regions where malaria is or was common. The clinical manifestations of sickle cell anaemia in India is seen to be milder than in Africa & Jamaica. Sickle cell trait or carrier state occurs in 10-30% of many predominantly tribal population throughout central India. Chhattisgarh is newly created state of central India belonging mostly to tribal & backward classes where malaria is endemic in many pockets of state, a large population is sufferring from Sickle Cell Disease. 15% of population of Chhattisgarh being Sickle trait (AS) and 1.27% Sickle cell anaemia.

Signs & Symptoms

Fatigue, Anaemia, Pain, Dactylitis (swelling & inflammation of the hands and / or feet) Arthritis, Acute Chest Syndrome (Fever, chest pain, difficulty in breathing and, pulmonary infiltrate on chest X-ray), Bacterial Infections, Splenic sequestration, Hemolytic crisis, Liver congestion, In Sickle cell trait which is always asymptomatic, manifest as the renal concentrating defect presenting with isosthenuria.

Ayurvedic Perspective

Sickle cell disease can be compared with pandu vyadhi in ayurved. To understand the ayurvedic perspective of sickle cell disease we have to understand:-

Normal rakta utpatti, Hetu, Lakshana, Samprapti, Chikitsa Sidhant, Chikitsa  Dravya

NORMAL RAKTH UTPATTI

 

Shudha raktha utpatti

Shudha raktha utpatti

 

Samprapthi


Hetu

Aetiological factors.

-Indulging in excessive intake of

Salt (athi lavana), Alkali ( Kshar )

-Habitual intake of

Horse gram (kulatha), Black gram (mas ha), Legumes (nishpava),

Sesame oil (tila taila), Tubers (pindaalu),

Salads specially of  ( moolak)etc,

Animal flesh of aquatic (jalaj) and of marshy (aanup) origin,

Meat of animals living in holes (),

Meat of animals which snatch their food ()

-Excessive intake of

sour curd(),  vinegar ()

and other sour fermented liquids.

-Use of opposite qualities like milk products and non-veg () stale (), decomposed food items.

-Habitual day time sleeping after meals which are having qualities like unctuous, heavy to digest and liquid/fluid dominated meals.

-excessive intake of food,

excessive anger, exposure to sunlight and excessive direct wind.

-Suppressing urge of vomiting, avoiding bloodletting in specific period.

-Too much exertion, injury, indigestion, ingestion of food although there is prior indigestion, excessive meal, even though preceded.

-Naturally in the autumn.

Beej Dosh

यस्य यस्य ह्यवयवस्य बीजे बीजभागे वा दोषः प्रकोपमापद्यन्ते

तं तमवयवं विक्रुतिराविशाती

च शा ४!३०


बीजे इति कृत्स्न एवाराम्भके बीजे ! बीजभागे वेत्यवयवबीजस्य एकदेशे

चक्र च शा ४! ३०

यस्य यस्य ह्यवयवस्य बीजे बीजभागे वा दोषः प्रकोपमापद्यन्ते

तं तमवयवं विक्रुतिराविशाती

च. शा ४ l ३०


बीजे इति कृत्स्न एवाराम्भके बीजे ! बीजभागे वेत्यवयवबीजस्य एकदेशे

चक्र . च .शा ४ l ३०

CHIKITSA SIDHANTH


CHIKITSA DRAVYA

Amalaki,      Yashtimadhu,      Kutki,     Barangi,

Manjista,     Haridra,    Bakuchi,    Lodhra,    Lasuna,

Devadaru,     padma kashta,     raal,     usher,

jatamansi,     musta,     grandhiparni,     Nilika,     guduchi,

gambhari fala,      patala,      agnimantha,        sthuneyak,

laamanjak,      mashaparni,      vasa,      mahanimba,      madhusringi,

karpas patra,      vansha,      darbha,      sharpunkha,

duralabha,      mundi,       punarnava,

bringaraj,       bhramhi,      shringatak

CHIKITSA KALPA

Dadimadi ghruta,

Draksha Gruta,

taapyadi loha,

navayas loha,

dhatri avaleha,

mandoor vataka,

gomutra haritaki,

punarnava mandoor,

shilajit vataka,

guduchi swaras,

shatavaryadi gruta,

vasa gruta.

Diet in Sickle Cell Anaemia

A nutritional involvement in sickle cell anaemia has precedance in reports that this genetic disease is associated with high folic acid requirements.

Cyanate which inhibits sickling of RBC is formed as a product of the oxidation of thiocyanate. Hence thiocyanate may also be expected to possess anti-sickling value.

Diet containing thiocyanate – Cabbage – iRrkdksch] Cauliflower xksch, Raddish eqyh,

Turnip, Rapeseed (Mustard); Eggs of hen feed on Rapeseed meal has shown to be containing thiocyanate.

Nicosan a phytochemical useful in sickle cell anaemia is present in Sorghum bicolor (Jowar), Eugenia caryophyllum (Cloves), Pterocarpus osum, Piper guineenses.

Nitrilosides another phytochemical is present Sweet Potato, Spinach (Palak), Mung, Bamboo sprouts, Lentils (Masoor), Cassava, Black beans, Apple seeds, Blackberry, Eucalyptus leaves (Nilgiri), Millets

How can Sickle Cell Anemia Be Prevented?

You can’t prevent sickle cell anaemia because its an inherited disease. However you can take steps to reduce its complication

If you have sickle cell anaemia its important to

a)      Adopt or maintain a healthy lifestyle

b)      Take steps to prevent & control complication

c)      Learn way to cope with pain

Adopt / maintain healthy lifestyle

Follow healthy eating plan ie folic acid every day; 8 glasses of water which will help prevent dehydration. Regular physical activity to stay healthy (prevent over exercise). Enough sleep & rest Avoid smoking.

Prevent & Control Complication

Avoid decongestants such as pseudoephedrine. Avoid extreme heat or cold. Do not climb high altitudes without extra oxygen. Reduce stress. Avoid physical labor Vaccines to prevent infection. Regular hematological and medical checkups are compulsory. Learn sign & symptoms of major complications

Scope of future study

Role of shodhan before conception

Role of Raktabasti in sickle cell anaemia

Study of prevalence of sickle cell anaemia in doshaja prakruti and blood group.

Phytochemical study of drugs which are raktaprasadak and also acting on sarakta-meda in relation with sickle cell anaemia.

Follow

Get every new post delivered to your Inbox.

Join 48 other followers