Clinical Theory and Skills EMIs
Michael Reilly, Bangaru Raju in Extended Matching Items for the MRCPsych Part 1, 2018
Delayed gastric emptying.Does not gauge the size of other people correctly.Gauges her own size correctly.Gauges the size of inanimate objects correctly.Hypervitaminosis.Normal vitamin levels.Rapid gastric emptying.To make herself more attractive to others.To satisfy herself.Vitamin deficiencies.
Micronutrients
Chuong Pham-Huy, Bruno Pham Huy in Food and Lifestyle in Health and Disease, 2022
Since vitamin A is fat-soluble, it can be stored longtime in the body, primarily in the liver. Routine intake of large amounts of vitamin A supplements or polar bear liver over a period of time can result in toxic symptoms, including liver damage, bone fractures, joint pain, increased intracranial pressure, dizziness, alopecia (hair loss), headaches, vomiting, blurry vision, insomnia, fatigue, weight loss, drying of the mucous membranes, skin desquamation, coma, and even death (3, 9, 33, 56–58). Children are more sensitive than adults to a high retinol intake. These toxicities only occur with preformed vitamin A (retinoid), but not with carotenoids such as β-carotene. Hypervitaminosis A is usually a result of consuming too much preformed vitamin A from supplements or therapeutic retinoids (56). High intakes of preformed vitamin A supplement (more than 1,500 µg/day, only slightly higher than the RDA) can reduce bone mineral density, and increase fracture risk (56). In addition, there is also evidence that retinol is teratogenic (causing developmental malformation of the fetus and birth defect). Consequently, it has been suggested that pregnant women or those who are trying to become pregnant should not take vitamin A supplements and should not eat liver or liver products in high amounts (9, 33). Nevertheless, pregnant women are advised not to consume more than 3,000 µg/day (10,000 IU) vitamin A supplement to avoid risk of fetal toxicity (3, 33, 56). Consult a doctor before using vitamin A supplement if you are pregnant.
Vitamins
Stanley R. Resor, Henn Kutt in The Medical Treatment of Epilepsy, 2020
Prophylactic treatment may be beneficial for patients who are inactive, lack sufficient vitamin D in the daily usual diet, and are deprived of sunlight. After 6 months on AEDs such as PHT, PB, or CBZ, determination of calcium, phosphorus, and alkaline phosphatase levels is helpful. If there is suspicion of vitamin D deficiency, then a vitamin D level can also be measured. The average patient with epilepsy who is otherwise well on a normal diet probably does not need prophylactic vitamin D supplements. The symptoms of hypercalcemia from hypervitaminosis D or excessive calcium intake include weakness, nausea, vomiting, diarrhea, and obtundation. Nephrocalcinosis, nephrolithiasis, and metastatic calcification can ensue (29). If vitamin D or calcium is prescribed, then monitoring of the calcium, phosphorus, alkaline phosphatase, and creatinine should be done after a month, then every 3 months. Vitamin D and circulating 25-hydroxyvitamin D levels should be checked 1 month after starting such therapy, and then every 6 months (30).
Pseudotumor Cerebri Syndrome with Resolution After Discontinuing High Vitamin A Containing Dietary Supplement: Case Report and Review
Published in Neuro-Ophthalmology, 2018
Jason T. Chisholm, Michelle M. Abou-Jaoude, Amy B. Hessler, Padmaja Sudhakar
One of the most well-established secondary causes of PTCS is hypervitaminosis A, and there is good evidence that this syndrome can be induced if enough vitamin A is ingested.6,19 Studies have found serum vitamin A levels, in the form of retinol, to be significantly higher in idiopathic PTCS patients,20,21 and others have found significantly higher retinol levels in the cerebrospinal fluid as well.21–23 In 2007, Warner et al. found that the ratio of retinol to retinol binding protein (RBP) in the CSF was higher in patients with PTCS and was >1.0, suggesting the presence of unbound retinol, which they theorized may be toxic to arachnoid villi and lead to impaired CSF resorption.21 Increased RBP in the serum of individuals with PTCS has been reported in two studies, suggesting that the unbound toxic retinol in the CSF may be due to insufficient RBP transfer into the CSF compartment.21,24
Hypervitaminosis D without toxicity
Published in Baylor University Medical Center Proceedings, 2020
Jasmin Rahesh, Victoria Chu, Alan N. Peiris
Vitamin D deficiency is a common problem, with a prevalence of approximately 37% in US adults.1 Reasons for this high prevalence may include inadequate sunlight exposure and poor dietary intake of vitamin D. Vitamin D status is best assessed by 25(OH)D levels. Physician-prescribed vitamin D is one source of replenishing 25(OH)D vitamin D levels. However, vitamin D can also be purchased over the counter (OTC). These OTC products are not regulated by the Food and Drug Administration (FDA), and wide variations in content may be seen. Excessive intake of vitamin D appears to be a growing risk and can result in toxicity.2 This is only rarely a dispensing error.3 Marked hypervitaminosis D without toxicity has rarely been reported. We describe marked hypervitaminosis D in a woman without clinical or biochemical manifestations of toxicity, which resolved with cessation of OTC supplements.
Efficacy of B-vitamins and vitamin D therapy in improving depressive and anxiety disorders: a systematic review of randomized controlled trials
Published in Nutritional Neuroscience, 2023
Jaqueline G. Borges-Vieira, Camila K. Souza Cardoso
When it comes to vitamin D, it is critical to be aware that overdose can be toxic. Excessive supplementation for too long can inhibit parathyroid hormone (PTH), culminating in increased calcium absorption from the gastrointestinal tract and hypercalcemia. This condition can cause adverse effects such as nausea, vomiting, muscle asthenia, joint pains, polyuria, dehydration [116]. Due to hypervitaminosis D, the increased risk of tissue calcification, especially of coronary vessels and heart valves, is investigated, but current findings remain controversial [117]. The current DRI [83] is 600 IU/day for 19–70 years, or 800 IU/day for 71 years and older, with the UL considered safe for an intake of 4,000 IU/day for men and women — although higher doses with individualized frequency can be performed in clinical practice under supervision [118]. Lastly, consider that Vitamin D supplementation should be based on the personal vitamin D response as some genetic variations (like the MTHFR gene on vitamins B) may also influence vitamin D metabolization and, thereby, the response to supplementation and the vitamin D status based on 25(OH)D3 serum measurements [119,120].
Related Knowledge Centers
- Dietary Reference Intake
- Food Fortification
- Hypervitaminosis A
- Toxicity
- Vitamin A
- Polyuria
- Vitamin
- Vitamin D
- Megavitamin Therapy
- Vitamin D Toxicity