Homeopathic Medicines for Adenoids

Homeopathic Medicines for Adenoids

Homeopathic Medicines for Adenoids

 

  1. Hydrastis,
  2. Calcarea Phosphorica,
  3. Baryta Carb,
  4. Cistus Canadensis,
  5. Tuberculinam,
  6. Agraphes Nutans.

 

 

Hydrastis:

Hydrastis is perfectly homoepathic to the totality of the symptoms produced by adenoid begotations it has the yellow mucous and general lymphoid hypertrophy.

Kali Bichromicum:

Highly recommended by Cooper, Clifton and others as a most efficacious remedy in adenoid begetations. It corresponds to the dyscrasia, which permits adenoid growths or tonsillar enlargement.

Calcarea Iodide may be used in cases which are febrile in nature.

Baryta Carbonica:

It is also a useful remedy, essentially in children who have recurring attacks of acute tonsillitis.

Cistus Canadensis:

In scrofulous or arthritic individuals who have adenoid vegetation. There is extreme sensitiveness to cold air, this is characteristic sensation of heat and dryness in the throat so intense that the patient must drink to relieve. Cold air inhaled causes distress in the throat.

Cistus:

Has a special affinity for the naso-pharynx.

Tuberculinim:

Adenoids are greatly benefited and often times permanently cured by a weekly dose of Tuberculinum or preferably Bacillinum.

Apraphis Nutans:

Obstruction of the nostrils from adenoids. Throat deafness. Deafness and deaf mutism, brcathes with mouth open. It is essentially a catorrhal remedya and acts specally on the glands connected with the nasal cavity and its use generally avoids adenoid surgery.

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Clinical Significance & Adenoid Faces

Adenoids facesSignificance:

Enlarged adenoid/adenoid hypertrophy can nearly become the size of a ping-pong ball and completely block airflow through the nasal passages.

Enlarged adenoid can obstruct the nasal airway enough to attack the voice without actually stopping nasal airflow altogether.

 

Adenoid Faces:

Enlargement of adenoids in children causes atypical appearance of the face, referred to as adenoid faces-features of adenoid faces include mouth breathing, elongated face, prominent incisors hypoplastic maxilla, short upper lip, elevated nostrils, high arched palate.

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Structure & Development Of Adenoid

Structure & Development Of Adenoid

Structure & Development Of Adenoid

Structure:

The adenoid has pseudostratified epithelium. The adenoid is often removed along with the palatine tonsils.

Development:

Adenoids develop from a subepithelial infiltration of lymphocytes after the 16th week of embryonic life.

They are part of Waldeyer Ring of Lymphnoid tissue which includes the palatine tonsils and the lingual tonsils.

After birth, enlargement begins and continues until aged 5 to 7 years. Symptomatic enlargement between 18-24 months of age is not uncommon meaning that snoring, nasal airway obstruction and obstructed breathing may occur during sleep.

The establishment of the upper respiratory tract is initiated at birth.

Species of bacteria such as lactobacilli anaerobic streptococci, actinomycosis, Fusobacterium species and Nocardia are normally present by 6 months of age. Normal flora found in the adenoids consists of alpha-hemolytic streptococci and entercocci.

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Adenoids

Adenoids

Adenoids

  1. Adenoids also known as pharyngeal tonsil / nasopharyngeal tonsil is a mass of lymphatic tissue situated posterior to the nasal cavity, in the roof of the nasopharynx, where the nose blends into the throat.
  2. Normally, in children it forms a soft mouth in the roof and posterior wall of the nasopharynx, just above and behind uvula.
  3. The adenoids are a mass soft tissue behind the nasal cavity. Like lymphnodes, adenoids are the past of the immune system and are made of the same type of tissues (Lymphoid Tissue).
  4. White blood cells circulate through the adenoids and other lymphnoid tissues reacting to foreign invaders in the body.
  5. We all have adenoids at birth and in childhood but as we head into adolscence they start to shrink.
  6. By adulthood, most people’s adenoids have disappeared.

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If The cause is unknown

fibrosis in IPF

fibrosis in IPF

The fibrosis in IPF has been linked to cigarette smoking, environmental factors (e.g. occupational exposure to gases, smoke, chemicals or dust.), and other medical complications including gastro intestinal reflex disease (GERD) or to genetic predisposition (Familial IPF).

IPF is the result of an aberrant wound healing process including, involving abnormal & excessive deposition of ‘Collagen’ (Fibrosis) in the pulmonary interstitium with minimal associated ‘inflamation’.

It is seen that the initial or repetitive injury in IPF appears to lung cells, called alveolar epithelial cells (AECs Pneumocytes), which line the majority of alveolar surface.

When type I AECs are damaged or last, it is through basement membranes.

In normal repair, the hyperplastic type II AECs die & remaining cells spread & undergo a differentiation process to become type I AECs.

Under pathologic conditions & in the presence of transforming growth factor beta (TGFB), fibroblasts accumulate in these areas of damage & differentiate myofibroblasts that secret collagen & other proteins.

The development of fibroblastic foci precedes the accumulation of inflammatory cells & the consequent deposition of collagen.

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Signs & Symptoms of IPF

Signs & Symptoms of IPF

Signs & Symptoms of IPF

Mostly the patient is over 50 years age.

The patient is having dry non productive cough.

Progressive exertional dyspnoea is seen.

Dry inspiratory bibasilar in ‘Velcro’ like crackers on auscultation is head in the patient. (A crackling in the lungs during inhalation during similar to Velcro being torn apart slowly that is heard with stethoscope)

Clubbing of digits, a disfigurement of the finger tips or toes is seen in IPF patients.

Abnormal pulmonary function test results, with evidence of restrictions & impaired gas exchange is seen in the IPF patient.

Symptoms are seen due to chronic oxygen deficiency in blood in IPF patients.

IPF patient with unexplained chronic exertional dyspnoea with cough, crackles, finger clubbing.

Cause of the IPF is mostly unknown, cigarette smoking & viral infection.

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Idiopathic Pulmonary Fibrosis

Idiopathic Pulmonary Fibrosis

It is chronic decline in lungs function. Pulmonary Fibrosis means scarring of lung’s tissues & is a cause of worsening dyspnoea (shortness of breathing).

Fibrosis is having poor prognosis.

Cause of IPF is unknown.

It mostly occurs in patients in between 50 to 70 years. It mostly occurs with history of cigarette smoking. It occurs more in men than women. In IPF(Idiopathic Pulmonary Fibrosis)more than 200 types of diseases are seen.

ILD (Interstitial Lung Diseases): In ILD the tissue between the air sacks in the lungs is primary sight of injury.

The interstitium, the air spores peripheral air ways & vessels are damaged in ILD.

Histopathology pattern- Usual interstitial Pneumonia (UIP).

*UIP is pathologic counterpart of IPF.

For diagnosis High Resolution Computer Tomography (HRCT) is done.

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Schizophrenia (A mental disorder)

Schizophrenia(A mental disorder)

Schizophrenia

1. Schizophrenia is a mental disorder of an characterized by abnormal social behavior &  failure to recognize what is real.
2. Common symptoms are false beliefs, unclear or confused thinking, auditory hallucinations, reduced social engagement & emotional expression & inactivity.
3. Diagnosis is based on observed behavior & the person’s reported experiences.
4. Genetics & early environment as well as psychological & social processes, appears to be important, contributory factors.
5. Some recreational & prescription drugs appear to cause or worsen symptoms.
6. It is a chronic, severe & disabling brain disorders.
7. It affects above 1% of the population all over the world.
8. Schizophrenia patient may hear voices, other people don’t hear or believe that others are reading their minds, controlling their thoughts or plotting to harm.
9. Terrifying experiences can cause fearfulness without or extreme agitation.

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