Ikääntyneen identiteetin tukeminen perhehoidossa : yksilöllisesti yhdessä -tehtäväkansio perhehoidon tueksi

Opinnäytetyö pyrkii tuomaan esille perhehoidon mahdollisuuksia vaihtoehtona perinteisesti tunnetuille vanhuspalveluille. Opinnäytetyössä perhehoito tarkoittaa ikääntyneen siirtymistä omaisen luo asumaan tilanteessa, jossa kotona pärjääminen on käynyt haasteelliseksi. Pääpaino on ikääntyneen ja omaisen välisessä suhteessa sekä yhteisen, toimivan kodin luomisessa eikä perhehoito tässä vaadi välttämättä virallisia sopimuksia omais- tai perhehoitajuudesta. Opinnäytetyön tarkoituksena on tukea ikääntyneen identiteettiä asuinympäristön vaihtumisen kynnyksellä. Tukemisella pyritään ikääntyneen identiteetin vahvistamiseen sekä identiteetin muokkautumisen hyväksymiseen toimintakyvyn heikentyessä ja uuden asuinmuodon tullessa ajankohtaiseksi. Tavoitteena oli tuottaa tehtäväkansio käytännön materiaaliksi omaisille, jotta heidän olisi helpompi tukea perhehoidossa asuvia ikääntyneitä. Ikääntyneiden omien intressien tukeminen ja oman identiteetin sovittaminen uuteen ympäristöön, ikääntymisen tuomat haasteet huomioiden, vaatii kaikilta osapuolilta sopeutumista. Opinnäytetyön tarve perustuu alati muuttuvaan väestörakenteeseen sekä ikäihmisten sosiaali- ja terveyspalveluita koskeviin lakeihin. Valtakunnallisiin tavoitteisiin nähden vanhuspalvelurakenne on edelleen liian laitosvaltainen ja suurten ikäluokkien ikääntymisen myötä laitosasumiselle on keksittävä vaihtoehtoisia ratkaisuja. Toimeksiantajamme toimii perhehoitajana ikääntyneille omaisilleen rakennuttamassaan varsinaissuomalaisessa kodissa. Opinnäytetyö perehtyy perhehoidon haasteisiin teemahaastattelujen kautta. Teemahaastattelut tehtiin sekä perhehoitajalle että hänen kanssaan asuville ikääntyneille. Toimintaterapian viitekehyksen, tässä tapauksessa Inhimillisen toiminnan mallin (Model of Human Occupation), sekä edellä mainittujen haastattelujen pohjalta koostettiin Yksilöllisesti Yhdessä tehtäväkansio. Opinnäytetyön tuotoksena syntynyt tehtäväkansio on luotu työvälineeksi omaisten ja ikääntyneiden välille, arkisten tilanteiden kohtaamiseen. Valmis tehtäväkansio lähetettiin haastatelluille pilotoitavaksi palautelomakkeiden kera, joiden avulla pyrittiin kartoittamaan, kohtaavatko tehtäväkansion tarjoama tuki ja perhehoidon tarpeet toisensa.This thesis aspires to raise awareness of the possibilities of family foster care as an alternative to more traditional care forms for senior citizens. It also aims to support the identity of the elderly as they transition to a new residential form. In this thesis family foster care refers to the situation in which a senior citizen moves in with their relative, when living at home alone becomes too much of a challenge. The focus in this kind of family foster care is in the relationship between the senior and their relative. In addition, creating a joint and functional home for all is important. This kind of family foster care does not require any official agreements of caregiving. The purpose of this thesis is to help support the identity of the elderly as their residential form and their surrounding environment changes. The goal is to reinforce the senior’s identity and to help them come to terms with their modifying identity as their performance capacity decreases and the new residential form in family foster care becomes a reality. The goal is to provide a task folder as concrete material for practical use so that the relatives of the elderly have something to help them in supporting their loved ones. Supporting the elderly with their own interests and finding their own identity is important. Furthermore, the elderly may face difficulties when adapting to the new environment, while taking notice of the challenges brought by aging. The need for this thesis is based on the constantly changing population structures and the laws concerning the health and social services of the elderly in Finland. In relation to the aims of the government, the structures of elderly care are still too institutionalized, and as the large age groups continue to age, the situation is forcing us to find alternative solutions. The employer of this thesis provides a home for her elderly relatives in a house in southwestern Finland she has built precisely with family foster care in mind. This thesis considers the challenges of family foster care through thematic interviews, which were conducted to the residents of the aforementioned home. The occupational therapy framework, in this case the Model of Human Occupation (MOHO), and the interviews mentioned before were used as groundwork in creating the task folder. The task folder was created to help the foster care families confront everyday challenges in their new living environment. The task folder was sent to the interviewees for testing with feedback forms. From the collected feedback it is possible to determine whether the support provided by the task folder met the challenges of family foster care

No signs of progressive beta cell damage during 20 years of prospective follow-up of autoantibody-negative diabetes.

Both type 1 and type 2 diabetes are considered to be associated with different degrees of progressive beta cell damage. However, few long-term studies have been made. Our aim was to study the clinical course of 20 years of diabetes disease, including diabetes progression, comorbidity, and mortality in a prospectively studied cohort of consecutively diagnosed diabetic patients. Among all 233 patients diagnosed with diabetes during 1985-1987 in Malmö, Sweden, 50 of 118 surviving patients were followed-up after 20 years. The age at diagnose was 42.3 ± 23.1 and 57.5 ± 13.6 years for antibody-positive and antibody-negative patients, respectively. HbA1c and plasma lipids were analyzed with regard to metabolic control. Islet antibody-negative patients at diagnosis had highly preserved C-peptide levels after 20 years in contrast to antibody-positive patients (antibody negative: C-peptide 0 years 0.78 ± 0.47 and 20 years 0.70 ± 0.46 (nmol/l), P = 0.51 and antibody positive: C-peptide 0 years 0.33 ± 0.35 and 20 years 0.10 ± 0.18; P < 0.001. Islet antibodies but not age, BMI, or C-peptide at diagnosis were predictors of C-peptide levels at 20 years when analyzed by logistic regression (P < 0.05). HbA1c did not differ between the groups after 20 years. The 20-year mortality was higher among antibody-negative patients, dependent on the higher age at diagnosis in this group (number of deaths: antibody positive: 18 of 56 vs. antibody negative: 109 of 188, P < 0.001). Of the deceased, 79% had died from diseases or complications that may be associated with diabetes. We found no progressive beta cell damage in autoantibody-negative diabetes at a 20-year follow-up of the clinical course of diabetes

Can complement factors 5 and 8 and transthyretin be used as biomarkers for MODY 1 (HNF4A-MODY) and MODY 3 (HNF1A-MODY)?

Aims Genetic testing is needed for the formal diagnosis of maturity-onset diabetes of the young (MODY), but this is not widely available. If any MODY biomarkers were known, these could possibly be used as an alternative. Hepatocyte nuclear factor (HNF)-1alpha and HNF-4alpha regulate transcription of genes encoding complement 5 (C5), complement 8 (C8) and transthyretin (TTR), suggesting that these could be potential biomarkers for the disease. We therefore set out to determine whether serum concentrations of C5, C8 and TTR can be used as biomarkers for patients with HNF4A-MODY and HNF1A-MODY. Methods The serum concentrations of C5, C8 and TTR were analysed in patients with mutations in the HNF-1alpha (n = 29) and EtaNuF-4alpha (n = 13) genes. Type 2 diabetic (n = 14) and healthy subjects (n = 20), matched for body mass index (BMI), served as diabetic and non-diabetic control groups, respectively. Results Type 2 diabetic patients had markedly increased levels of C5 and C8 compared with healthy control subjects. Levels of C5 and C8 correlated with glycated haemoglobin (C5: r = 0.48, P = 0.019). After adjustment for BMI, glycated haemoglobin, age and gender, HNF4A-MODY and HNF1A patients had reduced levels of C5 and C8 compared with Type 2 diabetic patients (C5: P = 0.001; C8: P = 0.004). In addition, patients with HNF4A-MODY, but not those with HNF1A-MODY, had decreased TTR compared with diabetic patients (P = 0.038). Conclusions Serum concentrations of C5 and C8 seem to distinguish HNF4A and HNF1A-MODY from other forms of diabetes. However, hyperglycaemia per se increases the serum concentrations, thereby attenuating their potential role as biomarkers for MODY

Characterization of beta cell and incretin function in patients with MODY1 (HNF4A MODY) and MODY3 (HNF1A MODY) in a Swedish patient collection.

The aim of this study was to evaluate the beta cell and incretin function in patients with HNF4A and HNF1A MODY during a test meal. Clinical characteristics and biochemical data (glucose, proinsulin, insulin, C-peptide, GLP-1 and GIP) during a test meal were compared between MODY patients from eight different families. BMI-matched T2D and healthy subjects were used as two separate control groups. The early phase of insulin secretion was attenuated in HNF4A, HNF1A MODY and T2D (AUC0-30 controls: 558.2 ± 101.2, HNF4A MODY: 93.8 ± 57.0, HNF1A MODY: 170.2 ± 64.5, T2D: 211.2 ± 65.3, P < 0.01). Markedly reduced levels of proinsulin were found in HNF4A MODY compared to T2D and that tended to be so also in HNF1A MODY (HNF4A MODY: 3.7 ± 1.2, HNF1A MODY: 8.3 ± 3.8 vs. T2D: 26.6 ± 14.3). Patients with HNF4A MODY had similar total GLP-1 and GIP responses as controls (GLP-1 AUC: (control: 823.9 ± 703.8, T2D: 556.4 ± 698.2, HNF4A MODY: 1,257.0 ± 999.3, HNF1A MODY: 697.1 ± 818.4) but with a different secretion pattern. The AUC insulin during the test meal was strongly correlated with the GIP secretion (Correlation coefficient 1.0, P < 0.001). No such correlation was seen for insulin and GLP-1. Patients with HNF4A and HNF1A MODY showed an attenuated early phase of insulin secretion similar to T2Ds. AUC insulin during the test meal was strongly correlated with GIP secretion, whereas no such correlation was seen for insulin and GLP-1. Thus, GIP may be a more important factor for insulin secretion than GLP-1 in MODY patients

A variant in the transcription factor 7-like 2 (TCF7L2) gene is associated with an increased risk of gestational diabetes mellitus.

Aims/hypothesis Genetic and epidemiological studies suggest an association between gestational diabetes mellitus and type 2 diabetes. Both are polygenic multifactorial disorders characterised by beta cell dysfunction and insulin resistance. Our aim was to investigate whether common genetic variants that have previously been associated with type 2 diabetes or related phenotypes would also confer risk for gestational diabetes mellitus. Materials and methods In 1,881 unrelated pregnant Scandinavian women (649 women with gestational diabetes mellitus, 1,232 non-diabetic control subjects) we genotyped the transcription factor 7-like 2 (TCF7L2 rs7903146), adiponectin (ADIPOQ +276G>T), peroxisome-proliferator activated receptor, gamma 2 (PPARG Pro12Ala), PPARGcoactivator, 1 alpha (PPARGC1A Gly482Ser), forkhead box C2 (FOXC2 −512C>T) and β3-adrenergic receptor (ADRB3 Trp64Arg) polymorphisms using TaqMan allelic discrimination assay or RFLP. Results The CC, CT and TT genotype frequencies of the TCF7L2 rs7903146 variant differed significantly between women with gestational diabetes mellitus and control women (46.3, 43.6 and 10.1% vs 58.5, 35.3 and 6.2%, p=3.7×10−6, corrected p value [Pc] for multiple testing Pc=2.2×10−5). The T-allele was associated with an increased risk of gestational diabetes mellitus (odds ratio 1.49 [95% CI 1.28–1.75], p=4.9×10−7 [Pc=2.8×10−6]). Compared with wild-type CC-genotype carriers, heterozygous (CT-genotype) and homozygous (TT-genotype) carriers had a 1.6-fold (95% CI 1.26–1.93, p=3.7×10−5 [Pc=0.0002]) and a 2.1-fold (95% CI 1.41–2.99, p=0.0001 [Pc=0.0008]) increased risk of gestational diabetes mellitus, respectively. The other polymorphisms studied were not significantly associated with gestational diabetes mellitus (ADIPOQ +276G>T: 1.17 [1.01–1.36], p=0.039 [Pc=0.23]; PPARG Pro12Ala: 1.06 [0.87–1.29], p=0.53; PPARGC1A Gly482Ser: 0.96 [0.83–1.10], p=0.54; FOXC2 −512C>T: 1.01 [0.87–1.16], p=0.94; and ADRB3 Trp64Arg: 1.22 [0.95–1.56], p=0.12). Conclusions/interpretation The TCF7L2 rs7903146 variant is associated with an increased risk of gestational diabetes mellitus in Scandinavian women

Alterations in bile acid synthesis in carriers of HNF1α mutations.

OBJECTIVES: Heterozygous mutations in hepatocyte nuclear factor 1α (HNF1α) cause maturity onset diabetes of the young 3 (MODY3), an autosomal dominant form of diabetes. Deficiency of HNF1α in mice results in diabetes, hypercholesterolaemia and increased bile acid (BA) and cholesterol synthesis. Little is known about alterations in lipid metabolism in patients with MODY3. The aim of this study was to investigate whether MODY3 patients have altered cholesterol and BA synthesis and intestinal cholesterol absorption. A secondary aim was to investigate the effects of HNF1α mutations on the transcriptional regulation of BA metabolism. METHODS: Plasma biomarkers of BA and cholesterol synthesis and intestinal cholesterol absorption were measured in patients with MODY3 (n = 19) and in matched healthy control subjects (n = 15). Co-transfection experiments were performed with several promoters involved in BA metabolism along with expression vectors carrying the mutations found in these patients. RESULTS: Plasma analysis showed higher levels of BA synthesis in MODY3 patients. No differences were observed in cholesterol synthesis or intestinal cholesterol absorption. Co-transfection experiments showed that one of the mutations (P379A) increased the induction of the cholesterol 7α-hydroxylase promoter compared to HNF1α, without further differences in other studied promoters. By contrast, the other four mutations (L107I, T260M, P291fsinsC and R131Q) reduced the induction of the farnesoid X receptor promoter, which was followed by reduced repression of the small heterodimer partner promoter. In addition, these mutations also reduced the induction of the apical sodium-dependent bile salt transporter promoter. CONCLUSIONS: BA synthesis is increased in patients with MODY3 compared with control subjects. Mutations in HNF1α affect promoters involved in BA metabolism. This article is protected by copyright. All rights reserved

Impaired vibrotactile sense at low frequencies in fingers in autoantibody positive and negative diabetes.

Vibration thresholds in index and little finger pulps in subjects with autoantibody [GADA, IA-2A and/or ICA] positive and negative diabetes 20 years after diagnosis were higher than in age-matched controls at low frequencies (8 and 16Hz), irrespective of HbA1c values, indicating selective impairment of Meissner's corpuscles and/or their innervating axons