Using an Ishikawa diagram as a tool to assist memory and retrieval of relevant medical cases from the medical literature

<p>Abstract</p> <p>Studying medical cases is an effective way to enhance clinical reasoning skills and reinforce clinical knowledge. An Ishikawa diagram, also known as a cause-and-effect diagram or fishbone diagram, is often used in quality management in manufacturing industries.</p> <p>In this report, an Ishikawa diagram is used to demonstrate how to relate potential causes of a major presenting problem in a clinical setting. This tool can be used by teams in problem-based learning or in self-directed learning settings.</p> <p>An Ishikawa diagram annotated with references to relevant medical cases and literature can be continually updated and can assist memory and retrieval of relevant medical cases and literature. It could also be used to cultivate a lifelong learning habit in medical professionals.</p

Alexithymia may explain the relationship between autistic traits and eating disorder psychopathology

Background: Autistic people are disproportionately vulnerable to anorexia nervosa and other eating disorders (ED), and within the general population, autistic traits correlate with ED psychopathology. A putative mechanism which may underpin this heightened risk is alexithymia, a difficulty identifying and describing emotional states which is observed in both autism and ED. In two experiments with independent non-clinical samples, we explored whether alexithymia might mediate the heightened risk of eating psychopathology in individuals high in autistic traits. Methods: Our first experiment used the PROCESS macro for SPSS to examine relationships between alexithymia (measured by the Toronto Alexithymia Scale (TAS-20)), autistic traits (autism quotient (AQ)), and eating psychopathology (Eating Attitudes Test (EAT-26)) in 121 participants. Our second experiment (n = 300) replicated and furthered this analysis by examining moderating effects of sex and controlling for anxiety and depression as covariates. We also included an additional performance-based measure of alexithymia, the Levels of Emotional Awareness Scale (LEAS). Results: Study 1 suggested that TAS-20 scores mediated the relationship between heightened autistic traits and eating psychopathology. Replication and further scrutiny of this finding, in study 2, revealed that this mediation effect was partial and specific to the female participants in this sample. The mediation effect appeared to be carried by the difficulty identifying feelings subscale of the TAS-20, even when depression and anxiety were controlled for. LEAS scores, however, were not significantly related to autistic traits or eating psychopathology. Limitations: Cross-sectional data prevents any conclusions around the direction and causality of relationships between alexithymia, autistic traits, and eating psychopathology (alongside depression and anxiety), necessitating longitudinal research. Our non-clinical sample was predominantly Caucasian undergraduate students, so it remains to be seen if these results would extrapolate to clinical and/or autistic samples. Divergence between the TAS-20 and LEAS raises crucial questions regarding the construct validity of these measures. Conclusions: Our findings with respect to autistic traits suggest that alexithymia could partially explain the prevalence of ED in autistic people and may as such be an important consideration in the pathogenesis and treatment of ED in autistic and non-autistic people alike. Further research with clinical samples is critical to explore these ideas. Differences between men and women, furthermore, emphasize the importance of looking for sexspecific as well as generic risk factors in autistic and non-autistic men and women

Why kisspeptin is such important for reproduction?

Recently discovered neuropeptide called kisspeptin is thought to be an essential gatekeeper in control of reproduction. Kisspeptin, the product of KiSS-1 gene and its G protein-coupled receptor GPR54 play a master role in the puberty period and fertility. This 54 amino acid peptide known also as metastatin, because of its metastasis suppression ability is also implicated in tumour biology. Kisspeptin/GPR54 system activates the hypothalamus-pituitary-ovarian axis. Its mechanism is not clearly understood. Kisspeptin influence is found above more at the level of hypothalamus but also at the pituitary and ovaries level. Kisspeptin can directly stimulate GnRH secretion from arcuate nucleus of hypothalamus. It is thought that kisspeptin plays an essential role in the metabolic regulation of fertility. In negative energy balance conditions an expression of KiSS-1 gene is decreased. Inactivating GPR54 mutations cause hypogonadotropic hypogonadism in humans. Simultaneously, mutations which increase GPR54 signalling are connected with gonadotropin-dependent premature puberty. Lately, possible therapeutic role of kisspeptin administration has been discussed. It was stated that kisspeptin might be used to manipulate the hypothalamic-pituitary-gonadal axis in humans. However, further studies are essential to reveal the exact mechanism and role of GPR54 agonists and antagonists applications. Moreover, the role of kisspeptin in the aspect of detection and treatment of specific cancers should be discovered

Hypoestrogenism in young women and its influence on bone mass density

One of the most important hormonal factors responsible for bone health is estradiol. Genetic factors, adequacy of hormonal functioning, nutrition and physical activity may be the markers of bone status and development in young women. During adolescence, women reach peak bone acquisition and develop a skeletal mass. This process is largely regulated by endocrine factors mainly such as adequate levels of gonadal, adrenal and pituitary hormones. The crucial role played by estradiol and its impact on bones are very multiple. Estradiol induces growth factors' activation, receptor activator of nuclear factor kappa B ligand (RANKL) production inhibition and is mainly referred to antiresorptive activity. Clinical situations leading to hypoestrogenism has been linked to decreased bone mineral density leading to osteopenia and osteoporosis. This status both in fertile and perimenopausal women can increase the risk of pathological fractures. Such conditions as hypothalamic-pituitary insufficiency (functional hypothalamic amenorrhea, anorexia nervosa, Kallmann syndrome, hyperprolactinemia), ovarian failure (gonadal dysgenesis, premature ovarian failure) and iatrogenic treatment (surgery, chemotherapy, radiotherapy) can cause hypoestrogenism. The treatment of osteopenia and osteoporosis caused by hypoestrogenism is very essential and multidirectional. The crucial role of the therapy is the achievement of proper serum estradiol concentration and eliminate the causes of hypoestrogenism

New markers of insulin resistance in polycystic ovary syndrome

Polycystic ovary syndrome (PCOS) is the most common endocrine-metabolic disorder in women of reproductive age. The diagnostic criteria include two out of three features: hyperandrogenism, polycystic ovaries on ultrasound and menstrual irregularities (Rotterdam Criteria 2003). PCOS patients are more vulnerable to develop diabetes, cardiovascular diseases and metabolic syndrome. Insulin resistance (IR) is prevalent in women with PCOS independently of obesity and is critically involved in reproductive and metabolic complications of the syndrome. Several tests have been developed to measure IR, some very reliable but complex like the hyperinsulinemic euglycemic glucose clamp and others less precise but easier and less invasive like HOMA-IR. New markers are needed to reach a more reliable assessment of insulin resistance. To date, several surrogate markers have been proposed in the literature to facilitate and improve the determination of IR. Many new proteins are strongly involved with PCOS physiopathology and IR, such as some adipocytokines (adiponectin, visfatin, vaspin and apelin), copeptin, irisin, PAI-1 and zonulin. Many other proteins have been proposed as potential new markers of IR in PCOS, such as resistin, leptin, RBP4, kisspetin and ghrelin, but their role is still controversial. In this review, we provide a short characterization of these new markers, recently studied as indicators of metabolic state

Functional hypothalamic amenorrhea: current view on neuroendocrine aberrations

Functional hypothalamic amenorrhea (FHA) is defined as a non-organic and reversible disorder in which the impairment of gonadotropin-releasing hormone (GnRH) pulsatile secretion plays a key role. There are main three types of FHA: stress-related amenorrhea, weight loss-related amenorrhea and exercise-related amenorrhea. The spectrum of GnRH-luteinizing hormone (LH) disturbances in FHA is very broad and includes lower mean frequency of LH pulses, complete absence of LH pulsatility, normal-appearing secretion pattern and higher mean frequency of LH pulses. Precise mechanisms underlying the pathophysiology of FHA are very complex and unclear. Numerous neuropeptides, neurotransmitters and neurosteroids play important roles in the physiological regulation of GnRH pulsatile secretion and there is evidence that different neuropeptides may be involved in the pathophysiology of FHA. Particular attention is paid to such substances as allopregnanolone, neuropeptide Y, corticotropin-releasing hormone, leptin, ghrelin and beta-endorphin. Some studies reveal significant changes in these mentioned substances in patients with FHA. There are also speculations about use some of these substances or their antagonists in the treatment of FHA

Kisspeptin and LH pulsatile temporal coupling in PCOS patients

Purpose: To evaluate the temporal coupling between spontaneous kisspeptin and luteinizing hormone (LH) pulsatile releases in polycystic ovary syndrome (PCOS) patients. Methods: We examined 71 patients diagnosed with PCOS. A 2 h pulsatility study was performed to evaluate serum kisspeptin and LH pulse frequency and concentration, sampled every 10 min; baseline follicle-stimulating hormone (FSH), estradiol (E2), prolactin (PRL), cortisol, 17-hydroksy-progesterone (17OHP), testosterone (T), free testosterone index (FTI, and insulin levels were also measured. Detect and Specific Concordance (SC) algorithms were used to evaluate the temporal coupling associations between spontaneous episodic secretion of kisspeptin and LH. Results: All PCOS patients demonstrated LH and kisspeptin pulsatile secretions. When the SC index was calculated across the sample of PCOS patients (n = 71), no temporal coupling was observed between kisspeptin and LH pulses. When PCOS patients were subdivided according to their menstrual cyclicity, oligomenorrheic patients demonstrated elevated kisspeptin pulse frequency. Additionally, the SC index reveled a temporal coupling between kisspeptin and LH secretory peaks only in eumenorrheic patients (n = 30, intermenstrual interval &lt; 45 days). Oligomenorrheic PCOS patients (intermenstrual interval &gt; 45 days) did not demonstrate temporal coupling between kisspeptin and LH secretory peaks. Conclusions: The study of the endogenous kisspeptin and LH pulsatile release revealed the temporal coupling of kisspeptin with LH secretory pulses only in eumenorrheic. This data supports the hypothesis that neuroendocrine impairments in PCOS affect the coupling of kisspeptin with LH pulses and potentially worsen as the disease progresses, becoming unequivocally evident in oligomenorrheic PCOS patients