Ομοιοπαθητική Θεσσαλονίκη | omoiotherapeia.gr
Ομοιοπαθητική Θεσσαλονίκη | omoiotherapeia.gr
Ομοιοπαθητική Θεσσαλονίκη | omoiotherapeia.gr
Ομοιοπαθητική Θεσσαλονίκη | omoiotherapeia.grr
Ομοιοπαθητική Θεσσαλονίκη | omoiotherapeia.gr
Ομοιοπαθητική Θεσσαλονίκη | omoiotherapeia.gr
Ομοιοπαθητική Θεσσαλονίκη | omoiotherapeia.gr

MY HOMEOPATHIC TREATMENT

The first major feature of my Homeopathic Treatment is the Indivualization for Treatment Determination.This means that different people may have different pathogenic reasons,symptoms and syndromes even though the disease name is the same, so treatment strategies and formulas are different. So different treatment strategies will be used according to the different causative factors.

The other major principle is Totality for Treatment Determination.This means that in all Diseases the whole organism suffers,even if organ pathology is conventionally recognized in a certain organ or part of the body.So,treatment should be applied for both the diseased organ or part of the body and for the totality of all current sufferings all over the body.

 

Modern Homeopathy should care equally

for both the Patient and the Disease.

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Your First Appointment

Just after the booking of the Appointment and  before the Consultation,you are provided  via email with a printed Questionnaire,which must be completed.  It asks for:

    •Basic  contact details, including address, phone and mobile numbers, email address

    •A brief description  of  your current health problems

    •A brief reference to your past medical history

Try to complete the questionnaire well in advance of your appointment and bring to me at your consultation appointment

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MY HOMEOPATHIC CONSULTATION

The consultations take place in a comfortable, relaxed and friendly environment. The first time you come along for a consultation, I spend at least an hour talking through the specific symptoms,health conditions and/or disease(s) you have, obtaining all necessary details of your case history, including any relevant lab tests,medical records,etc that you might already have. During this time you will have a unique opportunity to talk in detail with me about these ailments.Any questions I ask will help me to get a good understanding of your physical and/or emotional problems.

 

Once Homeopathic treatment has started, follow-up appointments take place once every 4-8 weeks( usually every 6 weeks). During follow up appointments, it is assessed how you are getting on with the homeopathic remedies prescribed, the progress you have made according to homeopathic principles and any indicated extension of the homeopathic case taking is added and included. Further homeopathic medication is prescribed for you based on this evaluation.The whole process is about reviewing , re-formulating and proceeding the planned homeopathic treatment

 

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Health Conditions /

ACNE

Acne vulgaris (or simply acne) is a long-term skin disease that occurs when hair follicles become clogged with dead skin cells and oil from the skin. Acne is characterized by areas of blackheads, whiteheads, pimples, and greasy skin, and may result in scarring. The resulting appearance can lead to anxiety, reduced self-esteem and, in extreme cases, depression or thoughts of suicide.

 

The role of diet and cigarette smoking is unclear and neither cleanliness nor sunlight appear to be involved.Acne primarily affects skin with a greater number of oil glands, including the face, upper part of the chest, and back. During puberty, in both sexes, acne is often brought on by an increase in androgens such as testosterone. Excessive growth of the bacteria Propionibacterium acnes, which is normally present on the skin, is often involved

 

Acne is commonly classified by severity as mild, moderate, or severe. Mild acne is classically defined as open (blackheads) and closed (whiteheads) comedones limited to the face with occasional inflammatory lesions. Acne may be considered to be of moderate severity when a higher number of inflammatory papules and pustules occur on the face compared to mild cases of acne, and acne lesions also occur on the trunk of the body.Lastly, severe acne is said to occur when nodules (the painful 'bumps' lying under the skin) are the characteristic facial lesions, and involvement of the trunk is extensive

Large nodules have been referred to as cysts in the past, and the term nodulocystic has been used in the medical literature to describe severe cases of inflammatory acne. However, since true cysts are rare in those with acne, the term severe nodular acne is now the preferred terminology.

Signs and symptoms

 

Typical features of acne include seborrhea (increased oil secretion), microcomedones, comedones, papules, pustules, nodules (large papules), and in many cases scarring. The appearance of acne varies with skin color. It may result in psychological and social problems.

Scars

Acne scars are the result of inflammation within the dermal layer of skin, brought on by acne, and are estimated to affect 95% of people with acne vulgaris. The scar is created by an abnormal form of healing following this dermal inflammation. Scarring is most likely to occur with severe nodular acne, but may occur with any form of acne vulgaris.[24] Acne scars are classified based on whether the abnormal healing response following dermal inflammation leads to excess collagen deposition or collagen loss at the site of the acne lesion.

 

Atrophic acne scars are the most common type of acne scar and have lost collagen from this healing response. Atrophic scars may be further classified as ice-pick scars, boxcar scars, and rolling scars. Ice-pick scars are typically described as narrow (less than 2 mm across), deep scars that extend into the dermis. Boxcar scars are round or ovoid indented scars with sharp borders and vary in size from 1.5–4 mm across. Rolling scars are wider than icepick and boxcar scars (4–5 mm across) and have a wave-like pattern of depth in the skin.

 

Hypertrophic scars are less common, and are characterized by increased collagen content after the abnormal healing response. They are described as firm and raised from the skin. Hypertrophic scars remain within the original margins of the wound, whereas keloid scars can form scar tissue outside of these borders. Keloid scars from acne usually occur in men, and usually occur on the trunk of the body rather than the face.]

Pigmentation

 

Postinflammatory hyperpigmentation (PIH) is usually the result of nodular acne lesions. They often leave behind an inflamed red mark after the original acne lesion has resolved. PIH occurs more often in people with darker skin color.Pigmented scar is a common but misleading term, as it suggests the color change is permanent. Often, PIH can be prevented by avoiding aggravation of the nodule. These scars can fade with time. However, untreated scars can last for months, years, or even be permanent if deeper layers of skin are affected.

    Cause

Hormonal

Hormonal activity, such as occurs during menstrual cycles and puberty, may contribute to the formation of acne. During puberty, an increase in sex hormones called androgens causes the follicular glands to grow larger and make more sebum. Acne that first develops between the ages of 21 and 25 is uncommon. Several hormones have been linked to acne, including the androgens testosterone, dihydrotestosterone (DHT), and dehydroepiandrosterone sulfate (DHEA-S), as well as insulin-like growth factor 1 (IGF-1) and growth hormone (GH). Both androgens and IGF-1 seem to be essential for acne to occur, as acne does not develop in individuals with complete androgen insensitivity syndrome (CAIS) or Laron syndrome (insensitivity to GH, resulting in extremely low IGF-1 levels).

 

Medical conditions that commonly cause a high-androgen state, such as polycystic ovary syndrome, congenital adrenal hyperplasia, and androgen-secreting tumors, can cause acne in affected individuals. Conversely, people who lack androgenic hormones or are insensitive to the effects of androgens rarely have acne. An increase in androgen (and sebum) synthesis may also be seen during pregnancy. Acne can be a side effect of testosterone replacement therapy or of anabolic steroid use.Anabolic steroids are commonly found in over-the-counter bodybuilding supplements.

Infectious

 

Propionibacterium acnes (P. acnes) is the anaerobic bacterium species that is widely suspected to contribute to the development of acne, but its exact role in this process is not entirely clear.There are specific sub-strains of P. acnes associated with normal skin and others with moderate or severe inflammatory acne. It is unclear whether these undesirable strains evolve on-site or are acquired, or possibly both depending on the person. These strains have the capability of either changing, perpetuating, or adapting to the abnormal cycle of inflammation, oil production, and inadequate sloughing of dead skin cells from acne pores. One particularly virulent strain has been circulating in Europe for at least 87 years. Infection with the parasitic mite Demodex is associated with the development of acne. However, it is unclear whether eradication of these mites improves acne.

Diet

 

The relationship between diet and acne is unclear, as there is no high-quality evidence which establishes any definitive link. High-glycemic-load diets have been found to have different degrees of effect on acne severity by different studies. Multiple randomized controlled trials and nonrandomized studies have found a lower-glycemic-load diet to be effective in reducing acne.Additionally, there is weak observational evidence suggesting that dairy milk consumption is positively associated with a higher incidence and severity of acne. Effects from other potentially contributing dietary factors, such as consumption of chocolate or salt, are not supported by the evidence. Chocolate does contain varying amounts of sugar, which can lead to a high glycemic load, and it can be made with or without milk. There may be a relationship between acne and insulin metabolism, and one trial found a relationship between acne and obesity. Vitamin B12 may trigger skin outbreaks similar to acne (acneiform eruptions), or exacerbate existing acne, when taken in doses exceeding the recommended daily intake.

Smoking

The relationship between cigarette smoking and acne severity is unclear and remains a point of debate. Due to the observational nature of the evidence obtained from epidemiological studies, there are concerns that bias and confounding may have influenced the results. Certain medical literature reviews have stated cigarette smoking clearly worsens acne whereas others have stated it is unclear whether smoking is unrelated to, worsens, or improves acne severity. Due to the various known negative health effects of cigarette smoking, it is not recommended as an approach to improving the appearance of acne.

Psychological

 

Overall, few high-quality studies have been performed which demonstrate that stress causes or worsens acne. While the connection between acne and stress has been debated, some research indicates that increased acne severity is associated with high stress levels in certain settings (e.g., in association with the hormonal changes seen in premenstrual syndrome).

Pathophysiology

 

Acne vulgaris is a chronic skin disease of the pilosebaceous unit and develops due to blockages in the skin's hair follicles. These blockages are thought to occur as a result of the following four abnormal processes: a higher than normal amount of sebum production (influenced by androgens), excessive deposition of the protein keratin leading to comedone formation, colonization of the follicle by Propionibacterium acnes (P. acnes ) bacteria, and the local release of pro-inflammatory chemicals in the skin.

 

The earliest pathologic change is the formation of a plug (a microcomedone), which is driven primarily by excessive proliferation of keratinocytes in the hair follicle. In normal skin, the skin cells that have died come up to the surface and exit the pore of the hair follicle. However, increased production of oily sebum in those with acne causes the dead skin cells to stick together. The accumulation of dead skin cell debris and oily sebum blocks the pore of the hair follicle, thus forming the microcomedone. This is further exacerbated by the biofilm created by P. acnes within the hair follicle. If the microcomedone is superficial within the hair follicle, the skin pigment melanin is exposed to air, resulting in its oxidation and dark appearance (known as a blackhead or open comedone). In contrast, if the microcomedone occurs deep within the hair follicle, this causes the formation of a whitehead (known as a closed comedone).

 

Dihydrotestosterone (DHT) is the main driver of androgen-induced sebum production in the skin. Another androgenic hormone responsible for increased sebaceous gland activity is DHEA-S. Higher amounts of DHEA-S are secreted during adrenarche (a stage of puberty), and this leads to an increase in sebum synthesis. In a sebum-rich skin environment, the naturally occurring and largely commensal skin bacterium P. acnes readily grows and can cause inflammation within and around the follicle due to activation of the innate immune system.[1] P. acnes triggers skin inflammation in acne by increasing the production of several pro-inflammatory chemical signals (such as IL-1α, IL-8, TNF-α, and LTB4); IL-1α is known to be essential to comedone formation.

 

A major mechanism of acne-related skin inflammation is mediated by P. acnes's ability to bind and activate a class of immune system receptors known as toll-like receptors, especially toll-like receptor 2 (TLR2) and toll-like receptor 4 (TLR4). Activation of TLR2 and TLR4 by P. acnes leads to increased secretion of IL-8, TNF-α, and IL-1α.[35] Release of these inflammatory signals attracts various immune cells to the hair follicle including neutrophils, macrophages, and Th1 cells. IL-1α stimulates higher keratinocyte activity and reproduction, which in turn fuels comedone development. Sebaceous gland cells also produce more antimicrobial peptides, such as HBD1 and HBD2, in response to binding of TLR2 and TLR4.

 

An  inflammatory cascade typically leads to the formation of inflammatory acne lesions, including papules, infected pustules, or nodules. If the inflammatory reaction is severe, the follicle can break into the deeper layers of the dermis and subcutaneous tissue and cause the formation of deep nodules. Involvement of AP-1 in the aforementioned inflammatory cascade also leads to activation of matrix metalloproteinases, which contribute to local tissue destruction and scar formation

Diagnosis

 

There are several features that may indicate that a person's acne vulgaris is sensitive to hormonal influences. Historical and physical clues that may suggest hormone-sensitive acne include onset between ages 20 and 30; worsening the week before a woman's menstrual cycle; acne lesions predominantly over the jawline and chin; and inflammatory/nodular acne lesions.

 

Several scales exist to grade the severity of acne vulgaris, but no single technique has been universally accepted as the diagnostic standard. Cook's acne grading scale uses photographs to grade severity from 0 to 8 (0 being the least severe and 8 being the most severe). This scale was the first to use a standardized photographic protocol to assess acne severity; since its creation in 1979, Cook's grading scale has undergone several revisions. Leeds acne grading technique counts acne lesions on the face, back, and chest and categorizes them as inflammatory or non-inflammatory. Leeds scores range from 0 (least severe) to 10 (most severe) though modified scales have a maximum score of 12. The Pillsbury acne grading scale simply classifies the severity of the acne from 1 (least severe) to 4 (most severe).

Acne vulgaris (or simply acne) is a long-term skin disease that occurs when hair follicles become clogged with dead skin cells and oil from the skin. Acne is characterized by areas of blackheads, whiteheads, pimples, and greasy skin, and may result in scarring. The resulting appearance can lead to anxiety, reduced self-esteem and, in extreme cases, depression or thoughts of suicide.

Typical features of acne include seborrhea (increased oil secretion), microcomedones, comedones, papules, pustules, nodules (large papules), and in many cases scarring. The appearance of acne varies with skin color. It may result in psychological and social problems.

Acne scars are the result of inflammation within the dermal layer of skin, brought on by acne, and are estimated to affect 95% of people with acne vulgaris.The scar is created by an abnormal form of healing following this dermal inflammation. Scarring is most likely to occur with severe nodular acne, but may occur with any form of acne vulgaris. Acne scars are classified based on whether the abnormal healing response following dermal inflammation leads to excess collagen deposition or collagen loss at the site of the acne lesion.

 

Atrophic acne scars are the most common type of acne scar and have lost collagen from this healing response. Atrophic scars may be further classified as ice-pick scars, boxcar scars, and rolling scars. Ice-pick scars are typically described as narrow (less than 2 mm across), deep scars that extend into the dermis. Boxcar scars are round or ovoid indented scars with sharp borders and vary in size from 1.5–4 mm across. Rolling scars are wider than icepick and boxcar scars (4–5 mm across) and have a wave-like pattern of depth in the skin.

 

Hypertrophic scars are less common, and are characterized by increased collagen content after the abnormal healing response. They are described as firm and raised from the skin. Hypertrophic scars remain within the original margins of the wound, whereas keloid scars can form scar tissue outside of these borders. Keloid scars from acne usually occur in men, and usually occur on the trunk of the body rather than the face.

 

Postinflammatory hyperpigmentation (PIH) is usually the result of nodular acne lesions. They often leave behind an inflamed red mark after the original acne lesion has resolved. PIH occurs more often in people with darker skin color. Pigmented scar is a common but misleading term, as it suggests the color change is permanent. Often, PIH can be prevented by avoiding aggravation of the nodule. These scars can fade with time. However, untreated scars can last for months, years, or even be permanent if deeper layers of skin are affected. Daily use of SPF 15 or higher sunscreen can minimize pigmentation associated with acne.

Hormonal activity, such as occurs during menstrual cycles and puberty, may contribute to the formation of acne. During puberty, an increase in sex hormones called androgens causes the follicular glands to grow larger and make more sebum. Acne that first develops between the ages of 21 and 25 is uncommon. Several hormones have been linked to acne, including the androgens testosterone, dihydrotestosterone (DHT), and dehydroepiandrosterone sulfate (DHEA-S), as well as insulin-like growth factor 1 (IGF-1) and growth hormone (GH). Both androgens and IGF-1 seem to be essential for acne to occur, as acne does not develop in individuals with complete androgen insensitivity syndrome (CAIS) or Laron syndrome (insensitivity to GH, resulting in extremely low IGF-1 levels).

 

Medical conditions that commonly cause a high-androgen state, such as polycystic ovary syndrome, congenital adrenal hyperplasia, and androgen-secreting tumors, can cause acne in affected individuals. Conversely, people who lack androgenic hormones or are insensitive to the effects of androgens rarely have acne. An increase in androgen (and sebum) synthesis may also be seen during pregnancy. Acne can be a side effect of testosterone replacement therapy or of anabolic steroid use. Anabolic steroids are commonly found in over-the-counter bodybuilding supplements.

 

Propionibacterium acnes (P. acnes) is the anaerobic bacterium species that is widely suspected to contribute to the development of acne, but its exact role in this process is not entirely clear. There are specific sub-strains of P. acnes associated with normal skin and others with moderate or severe inflammatory acne. It is unclear whether these undesirable strains evolve on-site or are acquired, or possibly both depending on the person. These strains have the capability of either changing, perpetuating, or adapting to the abnormal cycle of inflammation, oil production, and inadequate sloughing of dead skin cells from acne pores. One particularly virulent strain has been circulating in Europe for at least 87 years.Infection with the parasitic mite Demodex is associated with the development of acne.However, it is unclear whether eradication of these mites improves acne.

 

The relationship between diet and acne is unclear, as there is no high-quality evidence which establishes any definitive link. High-glycemic-load diets have been found to have different degrees of effect on acne severity by different studies. Multiple randomized controlled trials and nonrandomized studies have found a lower-glycemic-load diet to be effective in reducing acne. Additionally, there is weak observational evidence suggesting that dairy milk consumption is positively associated with a higher incidence and severity of acne.Effects from other potentially contributing dietary factors, such as consumption of chocolate or salt, are not supported by the evidence. Chocolate does contain varying amounts of sugar, which can lead to a high glycemic load, and it can be made with or without milk. There may be a relationship between acne and insulin metabolism, and one trial found a relationship between acne and obesity. Vitamin B12 may trigger skin outbreaks similar to acne (acneiform eruptions), or exacerbate existing acne, when taken in doses exceeding the recommended daily intake.

Overall, few high-quality studies have been performed which demonstrate that stress causes or worsens acne. While the connection between acne and stress has been debated, some research indicates that increased acne severity is associated with high stress levels in certain settings (e.g., in association with the hormonal changes seen in premenstrual syndrome).

Acne Rosacea is a long term skin condition characterized by facial redness, small and superficial dilated blood vessels on facial skin, papules, pustules, and swelling. Rosacea typically begins as redness on the central face across the cheeks, nose, or forehead, but can also less commonly affect the neck, chest, ears, and scalp.In some cases, additional signs, such as semipermanent redness, dilation of superficial blood vessels on the face, red domed papules (small bumps) and pustules, red gritty eyes, burning and stinging sensations, and in some advanced cases, a red lobulated nose (rhinophyma), may develop.

Four rosacea subtypes exist,and a patient may have more than one subtype:

 

    Erythematotelangiectatic rosacea exhibits permanent redness (erythema) with a tendency to flush and blush easily. It is also common to have small, widened blood vessels visible near the surface of the skin (telangiectasias) and possibly intense burning, stinging, or itching. People with this type often have sensitive skin. Skin can also become very dry and flaky. In addition to the face, signs can also appear on the ears, neck, chest, upper back, and scalp.

    Papulopustular rosacea presents with some permanent redness with red bumps (papules); some pus-filled pustules can last 1–4 days or longer. This subtype is often confused with acne.

    Phymatous rosacea is most commonly associated with rhinophyma, an enlargement of the nose. Signs include thickening skin, irregular surface nodularities, and enlargement. Phymatous rosacea can also affect the chin (gnathophyma), forehead (metophyma), cheeks, eyelids (blepharophyma), and ears (otophyma). Telangiectasias may be present.

    In ocular rosacea, affected eyes and eyelids may appear red due to telangiectasias and inflammation, and may feel dry, irritated, or gritty. Other symptoms include foreign body sensations, itching, burning, stinging, and sensitivity to light. Eyes can become more susceptible to infection. About half of the people with subtypes 1–3 also have eye symptoms. Blurry vision and vision loss can occur if the cornea is affected.