Suda Çözünen Vitaminler (Vitaminler-I) 1002 Hücre Doku Gelişimi Quiz

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31 Questions

C vitamini eksikliğinin belirtileri arasında aşağıdakilerden hangisi bulunmaz?

Kemik kırılmaları

Hangi durumda C vitamini ihtiyacı normalden daha fazladır?

Sigara kullanımında

C vitamini takviyesinin koruyucu olabileceği hastalıklardan biri aşağıdakilerden hangisidir?

Kanser

C vitamini aşırı alımının uzun vadede hangi olumsuz etkilere neden olabilir?

Osteoporoz

Araştırmada bahsedilen vitaminlerin hangisi suda çözünürdür?

Riboflavin

Hangi vitaminin eksikliği durumunda dermatit, glossit gibi belirtiler görülebilir?

Pantotenikasid

Hangi suda çözünen vitaminin fazlalığı hipervitaminoza neden olabilir?

Askorbik asid

Hangi vitamin profilaktik olarak kullanılabilir ve koroner arter hastalığı riskini azaltabilir?

Vitamin E

Aşağıdakilerden hangisi piridoksin (Vitamin B6) eksikliğinin bir sonucu olamaz?

Bulantı

Niasin (Vitamin B3) eksikliği aşağıdaki hastalıklardan hangisine yol açabilir?

Dermatit, ishal, demans

Vitamin B12 eksikliği aşağıdaki durumlardan hangisine yol açabilir?

Sinir hasarı, pernisiyöz anemi, spinal kord hasarı

Folik asit (Folate) eksikliği aşağıdaki durumlardan hangisine yol açabilir?

Nöral tüp defektleri, megaloblastik anemi, DNA sentez bozukluğu

Hangisi tiyamin (Vitamin B1) ile ilgili yanlıştır?

Tiyamin emilimi ile ilgili olarak ileum ve jejunumda gerçekleşir.

Aşağıdakilerden hangisi Riboflavin (Vitamin B2) eksikliğinin bir belirtisi değildir?

Kas zayıflığı

Hangisi biyotin (Vitamin B7) eksikliğinin bir sonucu olabilir?

Dilin şişmesi

Niasin ile ilgili aşağıdakilerden hangisi yanlıştır?

Niasin, kolesterol ve trigliserid üretimini engelleyebilir.

Suda çözünen vitaminlerin genel özellikleri arasında aşağıdakilerden hangisi yanlıştır?

Suda çözünen vitaminlerin enerji üretimiyle ilgili olduğu bilinir.

Hangi durum suda çözünen vitamin eksikliğinin genel belirtilerinden biri değildir?

Yüksek tansiyon

Hangi suda çözünen vitaminin eksikliğinde motor koordinasyon kaybı yaşanabilir?

Niasin

Aşağıdaki suda çözünen vitaminlerden hangisi enerji üretimiyle ilgili değildir?

Vitamin K

C vitamini eksikliği durumunda aşağıdaki belirtilerden hangisi görülebilir?

Yaralar, süngerimsi dişetleri

Aşağıdakilerden hangisi C vitamini eksikliğinin bir sonucu olamaz?

Aritmi, kalp çarpıntısı

Aşağıdakilerden hangisi C vitamini alımının uzun vadede olumsuz etkilerindendir?

Sürekli yüksek düzeyde oksidasyon

Aşağıdakilerden hangisi C vitamini eksikliğinin bir belirtisi olabilir?

Görme kaybı

Tiyamin (Vitamin B1) eksikliği aşağıdaki durumlardan hangisine yol açabilir?

Nörolojik hasar, sinir sıkışması, konvülsiyon ve koma

Riboflavin (Vitamin B2) eksikliği sonucu aşağıdakilerden hangisi oluşabilir?

Göz problemleri, kornea iltihabı ve dermatit

Biyotin (Vitamin B7) eksikliği sonucu aşağıdakilerden hangisi görülebilir?

Dermatit, dildeki genişlemiş damarlar, his kaybı ve kabarıklık

Niasin (Vitamin B3) eksikliği sonucu aşağıdaki hastalıklardan hangisine yol açabilir?

Dermatit, ishal, demans ve ölüm

Folik asit (Folate) eksikliği sonucu aşağıdakilerden hangisi görülebilir?

Megaloblastik anemi

Pridoksin (Vitamin B6) eksikliği durumunda aşağıdakilerden hangisi oluşabilir?

Anemi, mesane taşları, hiperkalsemi

Kobalamin (Vitamin B12) eksikliği durumunda aşağıdakilerden hangisi oluşabilir?

Nörolojik hasar, omurilik ve periferik sinirlerde zarar

Study Notes

  • Tiyamin (Vitamin B1) is a pirimidin and tiazol ring compound. It is found in plants, microorganisms, meat, and cereals. It is absorbed in the ileum and jejunum, and is bound to albumin. In metabolism, it is converted to its active form (TPP) in the liver (pyrophosphokinase). The body contains 10% TTP, 80% TPP, and 10% TMP.

  • TPP plays a crucial role in the oxidative decarboxylation of aldehyde groups such as alfa-keto acids, piruvate, and branched-chain amino acids (leucine, isoleucine, valine). In deficiency, pentoses (sugars) and branched-chain amino acids accumulate. TPP deficiency can lead to neuronal damage, including nerve compression, convulsions, and coma.

  • It is also important in alcoholism, particularly in the development of Wernicke-Korsakoff syndrome, which is caused by a deficiency in TPP absorption and metabolism.

  • Riboflavin (Vitamin B2) exists in two active forms: FMN (flavin mononucleotide) and FAD (flavin adenine dinucleotide). Both forms act as a cofactor with metals such as iron. They have the ability to donate or accept two hydrogen atoms during oxidation-reduction reactions.

  • Riboflavin deficiency can lead to problems with ectodermal tissues, such as eye problems, inflammation of the cornea, and dermatitis. It can also cause inflammation of the sindirim canal and skeletal anomalies in the fetus.

  • Vitamin B3 (Niasin) is a nicotinic acid and nicotinamide derivative. It forms NAD (nicotinamide adenine dinucleotide) and NADP (nicotinamide adenine dinucleotide phosphate). Both forms play a role in oxidation-reduction reactions and act as the cofactor for dehydrogenase enzymes. Niacin is required in the daily intake of 15-25 mg, along with tryptophan.

  • Niasin deficiency can lead to pellagra, a disease characterized by dermatitis, diarrhea, dementia, and death. It can also inhibit the production of cholesterol and triglycerides, making it useful in the treatment of hyperlipidemia.

  • Biyotin (Vitamin B7) is a widespread imidazole derivative that plays a role in the carboxylation reaction. Biyotin deficiency is rare, but can cause problems with the skin, dilated blood vessels (glossitis), loss of sensation, and bulging.

  • Pridoksin (Vitamin B6) exists in the forms of pyridoxine, pyridoxal, and pyridoxamine. It is involved in transamination, decarboxylation, and racemization reactions. It is particularly important in the metabolism of amino acids and is found in higher amounts in plant-based foods.

  • Pridoksin deficiency can lead to various symptoms, including dermatitis, dilated blood vessels (glossitis), loss of sensation, bulging, and depression. It can also affect other systems, such as anemia (which can be caused by a decrease in hemoglobin synthesis if iron deficiency is present), mesane stones, and hyperglycemia.

  • Folik asit (Folate) is formed from beta-alanine or pantoic acid. It plays a role in the metabolism of serine, glycine, histidine, and other one-carbon donors. It is particularly important in the neural tube development of the fetus and is a cofactor for the transfer of one-carbon groups to various molecules, including serine, thymine, and purine nucleotides.

  • Folate deficiency can lead to a lack of folic acid, which can result in megaloblastic anemia due to the slow division of rapidly dividing cells, such as erythrocytes and myeloid cells. It can also occur in situations where there is an increased requirement for folic acid, such as pregnancy, lactation, and alcoholism, and in the case of anticonvulsant use or antineoplastic agent use. It is also common in individuals with inadequate folate absorption.

  • Folate deficiency can lead to a lack of purine synthesis, which can result in DNA synthesis being impaired. This can cause cells to remain in the S phase and can lead to megaloblastic anemia. Folate deficiency is often accompanied by Vitamin B12 and pridoksin deficiencies.

  • Kobalamin (Vitamin B12) is a corrin ring compound that contains cobalt. It is synthesized by microorganisms and is absorbed from the ileum after the R-factor and IF binding reactions. Metilkobalamin is the cofactor for the methenyltransferase enzyme that synthesizes methionine. Vitamin B12 deficiency can lead to a lack of IF and parietal cell function, which can result in pernicious anemia, which is characterized by the atrophy of the mucosa and the inability of the stomach to absorb vitamin B12.

  • Vitamin B12 deficiency can also lead to neurological damage, including damage to the spinal cord and peripheral nerves, and can cause a degenerative condition in SSS, PSS, and spinal cord.

  • Tiyamin (Vitamin B1) is a pirimidin and tiazol ring compound. It is found in plants, microorganisms, meat, and cereals. It is absorbed in the ileum and jejunum, and is bound to albumin. In metabolism, it is converted to its active form (TPP) in the liver (pyrophosphokinase). The body contains 10% TTP, 80% TPP, and 10% TMP.

  • TPP plays a crucial role in the oxidative decarboxylation of aldehyde groups such as alfa-keto acids, piruvate, and branched-chain amino acids (leucine, isoleucine, valine). In deficiency, pentoses (sugars) and branched-chain amino acids accumulate. TPP deficiency can lead to neuronal damage, including nerve compression, convulsions, and coma.

  • It is also important in alcoholism, particularly in the development of Wernicke-Korsakoff syndrome, which is caused by a deficiency in TPP absorption and metabolism.

  • Riboflavin (Vitamin B2) exists in two active forms: FMN (flavin mononucleotide) and FAD (flavin adenine dinucleotide). Both forms act as a cofactor with metals such as iron. They have the ability to donate or accept two hydrogen atoms during oxidation-reduction reactions.

  • Riboflavin deficiency can lead to problems with ectodermal tissues, such as eye problems, inflammation of the cornea, and dermatitis. It can also cause inflammation of the sindirim canal and skeletal anomalies in the fetus.

  • Vitamin B3 (Niasin) is a nicotinic acid and nicotinamide derivative. It forms NAD (nicotinamide adenine dinucleotide) and NADP (nicotinamide adenine dinucleotide phosphate). Both forms play a role in oxidation-reduction reactions and act as the cofactor for dehydrogenase enzymes. Niacin is required in the daily intake of 15-25 mg, along with tryptophan.

  • Niasin deficiency can lead to pellagra, a disease characterized by dermatitis, diarrhea, dementia, and death. It can also inhibit the production of cholesterol and triglycerides, making it useful in the treatment of hyperlipidemia.

  • Biyotin (Vitamin B7) is a widespread imidazole derivative that plays a role in the carboxylation reaction. Biyotin deficiency is rare, but can cause problems with the skin, dilated blood vessels (glossitis), loss of sensation, and bulging.

  • Pridoksin (Vitamin B6) exists in the forms of pyridoxine, pyridoxal, and pyridoxamine. It is involved in transamination, decarboxylation, and racemization reactions. It is particularly important in the metabolism of amino acids and is found in higher amounts in plant-based foods.

  • Pridoksin deficiency can lead to various symptoms, including dermatitis, dilated blood vessels (glossitis), loss of sensation, bulging, and depression. It can also affect other systems, such as anemia (which can be caused by a decrease in hemoglobin synthesis if iron deficiency is present), mesane stones, and hyperglycemia.

  • Folik asit (Folate) is formed from beta-alanine or pantoic acid. It plays a role in the metabolism of serine, glycine, histidine, and other one-carbon donors. It is particularly important in the neural tube development of the fetus and is a cofactor for the transfer of one-carbon groups to various molecules, including serine, thymine, and purine nucleotides.

  • Folate deficiency can lead to a lack of folic acid, which can result in megaloblastic anemia due to the slow division of rapidly dividing cells, such as erythrocytes and myeloid cells. It can also occur in situations where there is an increased requirement for folic acid, such as pregnancy, lactation, and alcoholism, and in the case of anticonvulsant use or antineoplastic agent use. It is also common in individuals with inadequate folate absorption.

  • Folate deficiency can lead to a lack of purine synthesis, which can result in DNA synthesis being impaired. This can cause cells to remain in the S phase and can lead to megaloblastic anemia. Folate deficiency is often accompanied by Vitamin B12 and pridoksin deficiencies.

  • Kobalamin (Vitamin B12) is a corrin ring compound that contains cobalt. It is synthesized by microorganisms and is absorbed from the ileum after the R-factor and IF binding reactions. Metilkobalamin is the cofactor for the methenyltransferase enzyme that synthesizes methionine. Vitamin B12 deficiency can lead to a lack of IF and parietal cell function, which can result in pernicious anemia, which is characterized by the atrophy of the mucosa and the inability of the stomach to absorb vitamin B12.

  • Vitamin B12 deficiency can also lead to neurological damage, including damage to the spinal cord and peripheral nerves, and can cause a degenerative condition in SSS, PSS, and spinal cord.

Bu quiz, suda çözünen vitaminlerin genel özellikleri ve metabolizma süreçleri hakkında temel bilgiler sunmaktadır. Doç. Dr. Cem Horozoğlu'nun konuyla ilgili sunumundan esinlenilerek hazırlanmıştır.

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