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​​📌  Impetigo

🔸Introduction
 
Impetigo is a common, highly contagious superficial bacterial skin infection, primarily affecting children. It is caused by Staphylococcus aureus and Streptococcus pyogenes and manifests in two forms: nonbullous and bullous. The disease is prevalent worldwide, with a significant burden in low-income and tropical regions.

🔸Key Insights

Global Prevalence and Demographics:
·       Impetigo affects over 140 million people globally, with a higher incidence in children, particularly those aged 2 to 5 years (1, 3, 4, 6).
·       The prevalence is notably higher in underprivileged and marginalized communities, even in high-income countries (1).

Clinical Presentation and Diagnosis:
·       Nonbullous impetigo, caused by both S. aureus and S. pyogenes, is more common (70%) and typically presents with honey-colored crusted lesions (3, 4, 6).
·       Bullous impetigo, caused exclusively by S. aureus, is characterized by flabby bullae that rupture easily (3, 4, 6).
·       Diagnosis is primarily clinical, based on the appearance of characteristic lesions (3, 4, 6).

Treatment Guidelines and Antimicrobial Resistance:
·       Topical antibiotics are recommended for localized impetigo, while oral antibiotics are reserved for extensive cases (2-6).
·       There is a growing concern about antimicrobial resistance, particularly to commonly used topical agents, necessitating the use of systemic antibiotics in some regions (5, 8, 9, 10).
·       Guidelines vary internationally, with some not including recommendations for non-antibiotic treatments like antiseptics (2).

Epidemiology and Risk Factors:
·       Impetigo is more prevalent in warm, humid climates and is associated with poor hygiene, poverty, and co-infections like scabies (3, 4, 6, 7).
·       The lower limbs, distal upper limbs, face, and scalp are the most commonly affected areas (7).

Complications and Long-term Impact:
·       While generally mild, untreated impetigo can lead to serious complications such as acute post-streptococcal glomerulonephritis and chronic heart and kidney diseases (3, 4, 6, 8).

🔸Conclusion

Impetigo remains a significant global health issue, particularly affecting children in low-income and tropical regions. The disease is primarily managed with topical antibiotics, but rising antimicrobial resistance is a growing concern. Effective management requires adherence to treatment guidelines, awareness of local resistance patterns, and consideration of alternative therapies to mitigate the spread of resistant bacteria. Enhanced hygiene practices and public health strategies are crucial in reducing the prevalence and impact of impetigo.

📖 References

1.     https://doi.org/10.1371/journal.pone.0136789
2.     https://doi.org/10.1093/fampra/cmab066
3.     https://doi.org/10.1097/TME.0000000000000320
4.     https://doi.org/10.5937/galmed2203034k
5.     https://doi.org/10.36849/jdd.2020.4679
6.     https://doi.org/10.36713/epra13948
7.     https://doi.org/10.7717/peerj.14154
8.     https://doi.org/10.3390/antibiotics9120909
9.     https://doi.org/10.36849/JDD.2021.5795
10.   https://doi.org/10.1016/j.clinthera.2021.04.013


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📌 Rheumatic heart disease: Treatment

🔸 Introduction

Rheumatic heart disease (RHD) is a significant cause of cardiovascular morbidity and mortality, particularly in developing countries. It results from acute rheumatic fever and primarily affects the heart valves. Effective treatment strategies are crucial to manage symptoms, prevent disease progression, and improve patient outcomes.

🔸 Key Insights

Anti-inflammatory Treatment for Acute Rheumatic Fever:
·       Corticosteroids and intravenous immunoglobulins show little evidence of benefit in reducing the risk of heart valve lesions in patients with acute rheumatic fever. The studies are outdated and have a substantial risk of bias, necessitating new randomized controlled trials (1).
       
Medical Management:
·       Diuretics, angiotensin blockade, and beta-blockers are effective for symptom management and improving left ventricular function but do not alter disease progression (2).
·       Rhythm control for atrial fibrillation is preferred, with beta-blockers recommended for rate control when rhythm control is not possible. Anticoagulation is indicated for patients with a history of cardioembolism, atrial fibrillation, spontaneous left atrial contrast, and mechanical prosthetic valves (2, 7).

Secondary Antibiotic Prophylaxis:
·       Benzathine penicillin G (BPG) injections every four weeks are the cornerstone of secondary prevention, significantly reducing the risk of disease progression in children and adolescents with latent RHD (6,10).
·       High rates of BPG prescription and adherence are observed among patients retained in care, but retention itself is a significant barrier (3).
      
Surgical and Catheter-Based Interventions:
·       Definitive catheter and surgical interventions are the only treatments that can improve outcomes for patients with moderate or severe RHD. However, access to these interventions is limited in regions with high disease prevalence (4, 5, 8).
       
Management in Special Populations:
·       Pregnancy poses high risks for women with RHD, requiring careful management of anticoagulation and monitoring of disease progression (4, 9).
·       Patients with RHD are at increased risk of infective endocarditis, and antibiotic prophylaxis before procedures that may induce bacteremia is recommended, although evidence supporting this is limited (2, 10).

🔸 Conclusion

The treatment of rheumatic heart disease involves a combination of medical management, secondary antibiotic prophylaxis, and surgical interventions. While medications can manage symptoms and improve heart function, they do not halt disease progression. Secondary prophylaxis with benzathine penicillin G is crucial for preventing disease progression, especially in children and adolescents. Surgical and catheter-based interventions are necessary for severe cases but are often inaccessible in high-prevalence regions. Special considerations are required for managing RHD in pregnant women and preventing infective endocarditis. Overall, improving access to comprehensive care and retention in treatment programs is essential for better outcomes in RHD patients.

📖 References:
 
1.     https://doi.org/10.1097/CRD.0000000000000185
2.     https://doi.org/10.1002/14651858.CD003176.pub3
3.     https://doi.org/10.1161/CIRCOUTCOMES.117.004037
4.     https://doi.org/10.1016/j.pcl.2020.06.003
5.     https://doi.org/10.1016/S0140-6736(16)00547-X
6.     https://doi.org/10.1056/NEJMoa2102074
7.     https://doi.org/10.1016/j.ahj.2020.03.018
8.     https://doi.org/10.1016/b978-0-323-63982-8.00006-4
9.     https://doi.org/10.1161/CIR.0000000000000921
10.  https://doi.org/10.18773/austprescr.2022.034

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🎧 Treatment of Acute Upper Respiratory Infections: A Comprehensive Review (2015-2024)

Literary Source:

1. The Cochrane database of systematic reviews, 4 (2015): CD006821 . https://doi.org/10.1002/14651858.CD006821.pub3

2. Prescriber, 22. https://doi.org/10.1002/14651858.CD006895.pub3
 
3. Paediatric respiratory reviews (2020). https://doi.org/10.1016/j.prrv.2019.11.003
 
4. Italian Journal of Pediatrics, 41 (2015): A31 - A31. https://doi.org/10.1186/1824-7288-41-S2-A31
 
5. Bioscience trends, 13 2 (2019): 117-129 . https://doi.org/10.5582/bst.2018.01298
 
6. The Cochrane database of systematic reviews, 2, CD007880 . https://doi.org/10.1002/14651858.CD007880.pub3
 
7. The Cochrane database of systematic rev., 11, CD011360 . https://doi.org/10.1002/14651858.CD011360.PUB2
 
8. (2020). 22, 37-42. https://doi.org/10.26442/20751753.2020.11.200489
 
9. Infection & Chemoth. 49, 326 - 352. https://doi.org/10.3947/ic.2017.49.4.326
 
10. Am.fam. physician, 106 6, 628-636 . https://pubmed.ncbi.nlm.nih.gov/36521460/

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How to Choose the Ideal Diet for Your Body Type: tells Prof. G. Stechmann. Podcast

These questions are answered by Professor H. Stechmann:

1. How do you determine the ideal type of diet for different body types?
2. What kind of diet would you recommend for a 35-year-old woman with an endomorphic body type?
3. Can hormonal changes and age affect the choice of diet for a specific body type?
4. Are there any common mistakes that women often make when choosing a diet based on body type?
5. How to properly combine physical activity and diet based on body type to achieve the best results?
6. Is it possible to change your body type through diet, and if so, how?
7. How should individual characteristics, such as medical conditions or allergies, be taken into account when choosing a diet for one's body type?
8. What scientific research supports the link between body type and the effectiveness of various diets?
9. What would you advise women who are struggling to find the right diet and feel that their current plan is not working? What steps should they take?
10. What is the time interval between starting a particular diet and seeing visible results?

​​Paranoid Personality Disorder: How to Recognize and Manage Paranoia Effectively. >>>

These questions are answered by Prof. N. Schneider:

1. What is paranoid personality disorder and its primary symptoms?
2. What do people with paranoid personality disorder experience?
3. How common is paranoid personality disorder?
4. When do the first symptoms of paranoid personality disorder appear?
5. Are there differences in symptoms between men and women?
6. What risk factors contribute to developing paranoid personality disorder?
7. How much does genetics influence the development of paranoid personality disorder?
8. How is paranoid personality disorder diagnosed?
9. What are the most effective treatments for paranoid personality disorder?
10. How important is psychotherapy for treating paranoid personality disorder?
11. When and how can medications help treat paranoid personality disorder?
12. What is the prognosis for patients with timely treatment?
13. Can you summarize the key points about paranoid personality disorder and its treatment?

What is MAZOCHISM?

👉  Explains Prof. N. Schneider >>>

Duration: 31:06

Questions:

1. What is masochism and how does it differ from other forms of sexual behavior?

2. How does masochism differ from other sexual behaviors, particularly in terms of its focus on pain and humiliation?

3. How did Leopold von Sacher-Masoch’s life and work influence our understanding of masochism?

4. What are the primary psychological mechanisms that contribute to the development of masochistic tendencies?

5. Are there differences in how masochism manifests between men and women?

6. Why does pain become a source of sexual pleasure for some individuals?

7. What myths and misconceptions about masochism should be addressed?

8. Can masochism be part of a healthy sexual relationship? If so, how can it be incorporated positively?

9. What role do masochistic fantasies play in human life, and should they be regarded as normal?

10. How can people better understand and accept individuals with masochistic tendencies?

AARSKOG SYNDROME

( ending. For the beginning, see here>>> )

Different Opinions:

📌Aarskog syndrome can present with new oral-facial findings, including enamel dysplasia, a "col" deformity of the anterior mandible, and facial muscle paresis.
Melnick, M., & Shields, E. (1976). Aarskog syndrome: New oral‐facial findings. Clinical Genetics, 9. https://doi.org/10.1111/j.1399-0004.1976.tb01545.x.


📌Ophthalmic examination is crucial in asymptomatic patients with Aarskog syndrome to rule out treatable causes of visual loss.
Brodsky, M., Keppen, L., Rice, C., & Ranells, J. (1990). Ocular and systemic findings in the Aarskog (facial-digital-genital) syndrome.. American journal of ophthalmology, 109 4, 450-6 . https://doi.org/10.1016/S0002-9394(14)74612-4.


📌Aarskog's facial-digital-genital syndrome may be fairly common and early diagnosis through a syndrome identification centre could lead to earlier diagnosis of children with this and other syndromes.
Berry, C., CREE, A., & Mann, T. (1980). Aarskog's syndrome.. Archives of Disease in Childhood, 55, 706 - 710. https://doi.org/10.1136/adc.55.9.706.



📌Aarskog-Scott syndrome is associated with high prevalence of craniofacial, orthopaedic, and genitourinary tract clinical findings, but not directly related to underlying genotypes.
Drumond, V., Salgado, L., Salgado, C., Oliveira, V., Assis, E., Ribeiro, M., Valadão, A., & Orrico, A. (2021). The Prevalence of Clinical Features in Patients with Aarskog–Scott Syndrome and Assessment of Genotype-Phenotype Correlation: A Systematic Review. Genetics Research, 2021. https://doi.org/10.1155/2021/6652957.
 
 
📌Aarskog syndrome in a large Arabic family with a 2189delA mutation in the FDG1 gene shows clinical variability in cognitive skills, suggesting other genetic factors may play a role in phenotypic evolution.
Shalev, S., Chervinski, E., Weiner, E., Mazor, G., Friez, M., & Schwartz, C. (2006). Clinical variation of Aarskog syndrome in a large family with 2189delA in the FGD1 gene. American Journal of Medical Genetics Part A, 140A. https://doi.org/10.1002/ajmg.a.31033.
 
 
📌A new FGD1 gene variant has been identified in a Chinese family study, providing insights into the link between phenotype and genotype variations in Aarskog-Scott syndrome, aiding in diagnosis and treatment.
Liang, Y., Wu, H., He, X., & He, X. (2022). Case Report: Aarskog-scott syndrome caused by FGD1 gene variation: A family study. Frontiers in Genetics, 13. https://doi.org/10.3389/fgene.2022.932073.
 
 
📌Mutations in FGD1 gene may cause Aarskog-Scott syndrome, expanding the disease-causing mutation spectrum and highlighting the importance of considering neuropsychological phenotypes in patients.
Orrico, A., Galli, L., Cavaliere, M., Garavelli, L., Fryns, J., Crushell, E., Rinaldi, M., Medeira, A., & Sorrentino, V. (2004). Phenotypic and molecular characterisation of the Aarskog–Scott syndrome: a survey of the clinical variability in light of FGD1 mutation analysis in 46 patients. European Journal of Human Genetics, 12, 16-23. https://doi.org/10.1038/sj.ejhg.5201081.
 
 
📌Aarskog-Scott syndrome (AAS) is a rare developmental disorder with a complex phenotype and genetic heterogeneity, and next generation sequencing can potentially identify novel mutations underlying the condition.
Jabalameli, M., Briceño, I., Martinez, J., Pengelly, R., Ennis, S., & Collins, A. (2016). Aarskog-Scott syndrome: phenotypic and genetic heterogeneity. AIMS Genetics, 03, 049 - 059. https://doi.org/10.3934/genet.2016.1.49.
 
 
📌Aarskog syndrome (AS) is a complex, multisystemic disorder with wide phenotypic variability, and its diagnosis requires considering both primary and secondary criteria.
Teebi, A., Rucquoi, J., & Meyn, M. (1993). Aarskog syndrome: report of a family with review and discussion of nosology.. American journal of medical genetics, 46 5, 501-9 . https://doi.org/10.1002/AJMG.1320460508.

​​AARSKOG SYNDROME

Introduction

Aarskog Syndrome, also known as Aarskog-Scott Syndrome or Faciodigitogenital Syndrome, is a rare genetic disorder primarily affecting males. First described in 1970 by Norwegian pediatrician Dagfinn Aarskog and independently reported by Charles I. Scott Jr. in 1971, this syndrome features a combination of facial, skeletal, and genital anomalies, with possible growth delays and intellectual disabilities.

Frequency of Occurrence

Aarskog Syndrome is rare, affecting approximately 1 in 1 million individuals, primarily males. Females can be carriers and may show milder symptoms due to the X-linked recessive inheritance pattern.

Causes of the Disease

Aarskog Syndrome is caused by mutations in the FGD1 gene on the X chromosome. The FGD1 gene is crucial for normal cellular signaling and development. Mutations disrupt these processes, leading to the syndrome's characteristic features. The disorder follows an X-linked recessive inheritance pattern, affecting males who inherit the mutated gene and females who are typically carriers with mild symptoms.

Classification

Aarskog Syndrome features can be grouped into:

1. Facial Features: Widely spaced eyes (hypertelorism), drooping eyelids (ptosis), a short nose with a broad bridge, and a distinct facial appearance.
2. Skeletal Anomalies: Short fingers and toes (brachydactyly), curved fingers (clinodactyly), short stature, and joint abnormalities.
3. Genital Anomalies: Shawl scrotum, undescended testes (cryptorchidism), and other genital anomalies.
4. Growth and Developmental Issues: Growth delays, mild to moderate intellectual disabilities, and behavioral challenges.

Clinical Manifestations

The primary features of Aarskog Syndrome include:

1. Facial Features:
  - Hypertelorism (widely spaced eyes)
  - Ptosis (drooping eyelids)
  - Short, broad nose with a prominent bridge
  - Distinct facial appearance

2. Skeletal Anomalies:
  - Brachydactyly (short fingers and toes)
  - Clinodactyly (curved fingers)
  - Short stature
  - Joint abnormalities

3. Genital Anomalies:
  - Shawl scrotum
  - Cryptorchidism (undescended testes)
  - Hypospadias and other anomalies

4. Growth and Developmental Issues:
  - Growth delays
  - Intellectual disabilities
  - Behavioral challenges such as ADHD

Diagnosis

Diagnosing Aarskog Syndrome involves:

1. Clinical Examination: Identifying characteristic features.
2. Family History: Identifying affected individuals and carriers.
3. Genetic Testing: Confirming diagnosis by identifying mutations in the FGD1 gene.
4. Radiographic Studies: Assessing skeletal anomalies.
5. Developmental Assessment: Identifying intellectual disabilities and behavioral challenges.

Treatment

Management of Aarskog Syndrome includes:

1. Surgical Interventions: Correcting specific anomalies like cryptorchidism or hypospadias.
2. Developmental Support: Physical, occupational, and speech therapy, along with special education services.
3. Behavioral Therapy: Managing ADHD and other behavioral issues.
4. Medical Management: Regular evaluations and monitoring, possibly including growth hormone therapy.
Genetic Counseling: Understanding the genetic basis and risks for future pregnancies.

Prognosis

Prognosis varies with the severity of anomalies and effectiveness of interventions. With early diagnosis and comprehensive management, many individuals can lead relatively normal lives. Growth delays, intellectual disabilities, and behavioral challenges may persist, but targeted therapies can improve outcomes. Regular follow-up is essential for ongoing care and adjustment of management plans.

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