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Published in Henry J. Woodford, Essential Geriatrics, 2022
Thermoregulation becomes impaired as a consequence of frailty. Dysfunction of multiple physiological systems can contribute to this. Average core body temperature is estimated to be 0.4°C lower in older people compared to younger people.55 Core bodily temperature is a balance between heat creation from metabolism and heat loss from the skin, including evaporation of sweat. Blood flow to the skin is a key process in thermoregulation. The abilities to vasodilate and vasoconstrict are impaired in older people, making them more susceptible to hypothermia in cold conditions and overheating in hot settings. This is probably mediated by a reduction in sympathetic nervous system activity. Sweat production can be reduced when blood flow to the skin is impaired or with dehydration. Heat production is proportional to muscle mass, which declines with sarcopenia. Reduced activity can also result in less heat generation. There may be a reduced shivering response to hypothermia. Insulating fat conserves heat. There is a reduction in the subcutaneous fat layer in old age. Brown adipose tissue is important for thermogenesis in new-borns but probably not in adults. An underactive thyroid gland is a possible additional factor. Peripheral thermosensor receptors and central brain processing can be impaired in older age. There may also be cognitive aspects, such as wearing the appropriate clothing and home heating. Figure 22.1 summarises the aspects that promote hypothermia in frail older people. Paradoxical undressing can occur with hypothermia.56
General Practice Beginnings
Published in Peter Tate, Francesca Frame, Bedside Matters, 2020
In fact, the district nurses heroically dressed and coped with her ulcers, the social services department set up an efficient care package. They got her up in the morning, Meals on Wheels (‘Muck in a truck’ according to Mabel) fed her, the nurse assistant bed-bathed her regularly and someone came to put her to bed. My role as her doctor was very peripheral, but to her, still crucial. In her mind I was what stood between her and the grim reaper. To me, I wasn't sure what to do, medical school hadn't really equipped me for this long-term, pastoral sort of care, but I had been taught to do things, and so I did. I fiddled with her tablets. Someone, years ago, had diagnosed an underactive thyroid gland, and as she was always tired and sluggish, as well as being enormously overweight, I put her on a dose of thyroxine up to get things going. This gave me something to ask about when I visited.
The Endocrine System and Its Disorders
Published in Walter F. Stanaszek, Mary J. Stanaszek, Robert J. Holt, Steven Strauss, Understanding Medical Terms, 2020
Walter F. Stanaszek, Mary J. Stanaszek, Robert J. Holt, Steven Strauss
Located in the front part of the neck, the thyroid gland consists of two lateral lobes joined in front by a narrow band of tissue. The hormones secreted by the thyroid gland are thyroxin, triiodothyronine, and calcitonin. Its function is to regulate the rate of metabolism of the body cells. The thyroid gland also absorbs ingested iodine from the bloodstream for use in producing thyroxin.
Optimal thyrotropin level for low-risk papillary thyroid carcinoma after ultrasound-guided radiofrequency ablation
Published in International Journal of Hyperthermia, 2023
Xinyang Li, Lin Yan, Jing Xiao, Yingying Li, Yaqiong Zhu, Zhen Yang, Mingbo Zhang, Yukun Luo
Thyroid hormone therapy with levothyroxine is commonly used in the postoperative management of patients with differentiated thyroid cancer (DTC) to compensate for the lack of production by their thyroid glands [6]. Furthermore, thyroid stimulating hormone (TSH) has a growth effect on DTC, mediated by TSH receptors on the cell membrane [7]. TSH suppression using supraphysiological doses of levothyroxine could prevent progression or recurrence of thyroid cancers [4,8]. Such TSH suppression may improve outcomes in high-risk patients, but there is little evidence for this benefit in low-risk patients [9]. For patients with low-risk PTC undergoing lobectomy, the American Thyroid Association (ATA) guidelines recommend that TSH may be maintained in the mid to lower reference range (0.5–2mU/L) [4]. Consensus statements have suggested maintaining a low-normal TSH range during AS of low-risk PTC [10].
Radiobiological and social considerations following a radiological terrorist attack; mechanisms, detection and mitigation: review of new research developments
Published in International Journal of Radiation Biology, 2022
Tanya Kugathasan, Carmel Mothersill
Another type of agent given after the event of radiological exposure is mitigators. These are agents which can protect against some of the harmful effects by preventing or limiting the likelihood of adverse biological outcomes. An ideal mitigator would be orally ingested or a skin patch (Moulder 2014). However, radiation skin injuries make it quite problematic for the utilization of skin patches. It is important that the drugs used should have efficacy in multiple organ systems so that multiple drugs are not needed for different organ injuries (Moulder 2014). Angiotensin-converting enzyme inhibitors (ACEIs) were developed as hypertensive agents, however have found efficacy against a range of cardiac and renal diseases. Radioactive Iodine mostly raises concern due to the damage to the thyroid gland resulting in cancer or hyperthyroidism. This is commonly treated with the uptake of Sodium Iodide (NaI) or Potassium Iodide (KI). Iodine uptakes allow for a saturable process in the thyroid, hence preventing radioactive iodine from entering the thyroid (Anderson and Bokor 2013). The amount of dosage of KI depends on the age of the individual and the amount of natural iodine in the soil and hence the diet of exposed individuals. Infants between the ages of 1–3 have a dose intake of 32 mg, whereas adults have a dose intake of 130 mg (Anderson and Bokor 2013). It is still important to note however that KI does not protect against other internal radioisotopes or external radiation.
Toward a science-based testing strategy to identify maternal thyroid hormone imbalance and neurodevelopmental effects in the progeny – part I: which parameters from human studies are most relevant for toxicological assessments?
Published in Critical Reviews in Toxicology, 2020
Ursula G. Sauer, Alex Asiimwe, Philip A. Botham, Alex Charlton, Nina Hallmark, Sylvia Jacobi, Sue Marty, Stephanie Melching-Kollmuss, Joana A. Palha, Volker Strauss, Bennard van Ravenzwaay, Gerard Swaen
The thyroid gland is an endocrine organ present in all vertebrates. Thyroxine (T4) is the main thyroid hormone synthesised and secreted by the thyroid, whereas triiodothyronine (T3), the biologically active hormone, is mostly produced by deiodination of T4 in peripheral tissues. A major role of the thyroid hormones is to regulate metabolism, e.g. during growth and reproduction. In developing offspring, rodent data (with supporting evidence in humans) indicate that thyroid hormones play a role in neuronal migration, cellular differentiation (e.g. of neurons) and glial myelination. The thyroid gland is controlled by the pituitary [through secretion of thyroid stimulating hormone (TSH)] which, in turn, is regulated by the thyrotropin releasing hormone secreted by the hypothalamus (Dickhoff and Darling 1983; DeGroot and Jameson 2001). Thyroid hormones are highly hydrophobic and therefore generally bound to serum binding proteins when circulating in the bloodstream, whereas only a minor fraction (<1%) remains as free hormones (e.g. free T4 (fT4) and free T3). It is the free hormone fraction that is sensed by the tissues, triggering the homeostatic regulatory mechanisms (Stockigt 2001).