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"Mincer Pharma Antyalergiczny Kojący Krem CC do Twarzy Nr 1107 - Recenzja Produktu"
Recenzje 12
- Od najwyższej oceny
- Od najniższej oceny
- Sortowanie domyślne
- Od najstarszych
Dodanych produktów: 299
Napisanych recenzji: 594
5 / 5
2 listopada 2019, o 00:13
Używa produktu od: miesiąc
Wykorzystała: kilka próbek
Kupiony w: Otrzymałam w prezencie
Czyżby wycofany?
Przy okazji zakupów drogeryjnych udało mi się otrzymać kilka próbek tego produktu. Przyznaję, że przeleżały one w szafce, jednak ostatnio postanowiłam je w końcu wypróbować. Jedna saszetka o pojemności dwóch mililitrów starczyła mi na kilka zastosowań, tak więc jego wydajność wypadła naprawdę nieźle.
Kosmetyk nie posiada kompozycji zapachowej, co jest dobrym rozwiązaniem dla każdego typu cery, także tej wrażliwej, czy alergicznej.
Konsystencja jest średnio leista, a przy rozprowadzaniu gęstnieje na skórze. Bardzo dobrze zlewa się ona z naturalnym kolorem skóry, zapewniając jej delikatne krycie i pudrowe wykończenie. Kosmetyk utrwalałam dodatkowo pudrem, a całość utrzymała się przez cały dzień. Niewielkiej poprawki wymagała okolica nosa, która się jednak u mnie zawsze wyświeca, więc nie było to dla mnie niespodzianką. Tak czy inaczej, krem CC pozwolił mi na wyrównanie kolorytu skóry, z maskowaniem niedoskonałości. Kosmetyk nie powoduje efektu maski, wiec sprawdzi się dla osób ceniących delikatny, naturalny look. Dla mnie to strzał w dziesiątce, dlatego ubolewam, że nie mogę go dostać w żadnym sklepie- także internetowym :(
ZALETY: + brak kompozycji zapachowej
+ łatwość aplikacji
+ dobra trwałość, bez ścierania
+ pudrowe wykończenie
+ dobrze dopasowany odcień
+ lekkie krycie bez efektu maski
+ koryguje niedoskonałości
+ nie przesusza cery, nie wpływa negatywnie na jej stan
Dodanych produktów: 44
Introduction
Hashimoto thyroiditis is an autoimmune disease that destroys thyroid cells by cell and antibody-mediated immune processes. It is the most common cause of hypothyroidism in developed countries. In contrast, worldwide, the most common cause of hypothyroidism is an inadequate dietary intake of iodine. This disease is also known as chronic autoimmune thyroiditis and chronic lymphocytic thyroiditis. The pathology of the disease involves the formation of antithyroid antibodies that attack the thyroid tissue, causing progressive fibrosis. The diagnosis is often challenging and may take time until later in the disease process. The most common laboratory findings demonstrate elevated thyroid-stimulating hormone (TSH) and low levels of free thyroxine (fT4), coupled with increased antithyroid peroxidase (TPO) antibodies. However, earlier on in the course of the disease, patients may exhibit signs, symptoms, and laboratory findings of hyperthyroidism or normal values. This is because the destruction of the thyroid gland cells may be intermittent.
Women are more often affected. The female-to-male ratio is at least 10:1. Although some sources cite diagnosis happening more so in the fifth decade of life, most women are diagnosed between the ages of 30 to 50 years. Conventional treatment is comprised of levothyroxine at the recommended dose of 1.6 to 1.8 mcg/kg/day. The T4 converts to T3, which is the active form of thyroid hormone in the human body. Excessive supplementation can lead to deleterious and morbid effects, such as arrhythmias (the most common being atrial fibrillation) and osteoporosis. In this chapter, we review the pathogenesis, diagnosis, and management of Hashimoto thyroiditis.[1][2]
Differential Diagnosis
Hashimoto thyroiditis (HT) is one of the most frequent autoimmune diseases and has been reported to be associated with gastric disorders in 10% to 40% of patients. About 40% of patients with autoimmune gastritis also present with Hashimoto thyroiditis, according to research by Cellini et al. Chronic autoimmune gastritis (CAG) is characterized by the partial or complete disappearance of parietal cells leading to impairment of hydrochloric acid and intrinsic factor production. The patients go on to develop hypochlorhydria-dependent iron-deficient anemia, leading to pernicious anemia and severe gastric atrophy.
Thyrogastric syndrome was first described in the 1960s when thyroid autoantibodies were found in a subset of patients with pernicious anemia and atrophic gastritis. The latest guidelines have incorporated the two aforementioned autoimmune disorders into a syndrome now known as a polyglandular autoimmune syndrome (PAS). This is characterized by two or more endocrine and nonendocrine disorders. The thyroid gland develops from the primitive gut, and therefore the thyroid follicular cells share similar characteristics with parietal cells of the same endodermal origin. For example, both are polarized and have apical microvilli with enzymatic activity, and both can concentrate and transport iodine across the cell membrane via the sodium/iodide symporter. Iodine not only plays an essential role in the production of thyroid hormone, but it is also involved in the regulation of gastric mucosal cell proliferation and acts as an electron donor in the presence of gastric peroxidase, and assists in the removal of free oxygen radicals.
It is important to note that due to the pharmaceutical formation of thyroxine available worldwide, there can be problems with absorption in patients with disorders of the gastric mucosa. Most levothyroxine is obtained by salification with sodium hydroxide, making sodium levothyroxine. The absorption of T4 occurs in all areas of the small intestine and ranges from 62% to 84% of the ingested dose. Decreased gastric acid secretion can disrupt this percentage and may cause issues with decreased absorption of most pharmaceutical grade forms of levothyroxine, except for liquid-based or soft gel formations.
Histopathology
On pathologic examination, there is a diffuse, symmetric enlargement of the thyroid. The capsule is often intact with a prominent pyramidal lobe. When cut, the surface is similar to that of lymph nodes, with a pale brown to yellow color. Interlobular fibrosis may or may not be present. Atrophy may also occur, and in some patients, the gland may become nodular or asymmetric. However, necrosis or calcification does not occur and would suggest a different diagnosis.
The organ system manifestations of Hashimoto thyroiditis are varied due to the nature of the disease. Initially, patients may have bouts of hyperthyroid symptoms, as the initial destruction of thyroid cells may lead to the increased release of thyroid hormone into the bloodstream. Eventually, when enough destruction has been caused by the antibody response, patients exhibit symptoms of hypothyroidism. These symptoms are insidious and variable and may affect almost any organ system in the body.
The rate of hair growth slows, and hair can be dry, coarse, dull, and brittle. Diffuse or partial alopecia is not uncommon.
Decreased thyroid function can increase peripheral vascular resistance by as much as 50% to 60% and reduce cardiac output by as much as 30% to 50%. Bradycardia may result from a loss of chronotropic action of thyroid hormone directly on the sinoatrial cells. However, most patients have a few symptoms directly attributable to the cardiovascular system.
Fatigue, exertional dyspnea, and exercise intolerance are likely associated with a combination of limited pulmonary and cardiac reserve in addition to decreased muscle strength or increased muscle fatigue. Hypothyroid rats have been shown to have decreased endurance. Biochemical changes in this population have shown decreased muscle oxidation of pyruvate and palmitate, increased utilization of glycogen stores, and diminished fatty acid mobilization. Muscle weakness and myopathy are important features.
