Leptospirosis - clinical manifestations and diagnosis.pdfJim Jacob Roy
Leptospirosis is a commonly encountered infection , especially in tropical regions.
In this document , the clinical manifestations and diagnosis of leptospirosis is described.
The modified FAINE'S criteria is also described at the end.
Leptospirosis - clinical manifestations and diagnosis.pdfJim Jacob Roy
Leptospirosis is a commonly encountered infection , especially in tropical regions.
In this document , the clinical manifestations and diagnosis of leptospirosis is described.
The modified FAINE'S criteria is also described at the end.
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Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
Mastering Wealth: A Path to Financial FreedomFatimaMary4
### Understanding Wealth: A Comprehensive Guide
Wealth is a multifaceted concept that extends beyond mere financial assets. It encompasses a range of elements including money, investments, property, and other valuable resources. However, true wealth also includes non-material aspects such as health, relationships, and personal fulfillment. This guide delves into the various dimensions of wealth, exploring how it can be created, sustained, and enjoyed.
#### Defining Wealth
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#### The Importance of Financial Wealth
Financial wealth remains a critical component of overall wealth. It provides security, freedom, and the ability to pursue opportunities. Key elements of financial wealth include:
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2. **Investments**: Assets purchased with the expectation that they will generate income or appreciate over time. Common investments include stocks, bonds, mutual funds, real estate, and businesses.
3. **Income**: Regular earnings from work, investments, or other sources. Consistent income is essential for maintaining and growing wealth.
4. **Debt Management**: Effectively managing debt ensures that it does not erode financial wealth. This includes paying off high-interest debt and using credit wisely.
#### Creating Wealth
Creating wealth involves generating and accumulating financial and non-financial resources. The process can be broken down into several key strategies:
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EATING DISORDERS (Psychiatry-7)by dr Shivam sharma.pptxShivam Sharma
For any queries ,contact shvmshrm@outlook.com
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## Introduction to Eating Disorders
Welcome to this comprehensive presentation on Eating Disorders, a critical and often misunderstood area of mental health. This presentation is designed to provide in-depth knowledge and insights into the various aspects of eating disorders, making it valuable for both postgraduate medical aspirants preparing for the INI-CET and the general public seeking to understand these complex conditions.
### Objectives:
1. **Understanding Eating Disorders**: Gain a clear understanding of what eating disorders are, their types, and their distinguishing characteristics.
2. **Etiology and Risk Factors**: Explore the underlying causes and risk factors that contribute to the development of eating disorders.
3. **Clinical Features and Diagnosis**: Learn about the clinical features, diagnostic criteria, and the importance of early detection.
4. **Management and Treatment**: Review the current approaches to managing and treating eating disorders, including medical, psychological, and nutritional interventions.
5. **Prevention and Awareness**: Discuss strategies for prevention, early intervention, and increasing awareness about eating disorders.
This presentation aims to bridge the gap between academic knowledge and practical understanding, providing you with the tools to recognize, diagnose, and effectively manage eating disorders. Whether you are preparing for a medical exam or seeking to educate yourself or others about these serious conditions, this presentation will equip you with essential information and practical insights.
Let's begin our journey into understanding eating disorders and the significant impact they have on individuals and society.
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For any queries ,contact shvmshrm@outlook.com
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
2. Definition
It is characterized by sudden onset of gross hematuria,
edema, hypertension and deranged RFTs.
Most common Immune-mediated, glomerular inflammatory
disorder leading to acute kidney injury (AKI).
85 % of cases follow an infection by beta-hemolytic
streptococci.
3. It is classical self-limiting illness resulting from prior
pharyngeal or cutaneous infection with group beta-
hemolytic streptococci.
Alternative etiologies
S.pneumoniae (rare), S.aureus and other non-
streptococcal bacteria. Viral infections (e.g.EBV, parvovirus
B19)
4. Epidemiology
The disease burden is highest in resource-poor countries.
Incidence 9.5–28.5 new cases per 100,000 person-years.
Glomerulonephritis risk 5 % with pharyngitis and 25 % after
skin infection of nephritogenic S. pyogenes infections.
5. Pathogenesis
Exact mechanism of glomerular injury is debated
It though that to be an immune-complex mediated
disease.
Pattern of hypocomplementemia in AGN reflects
activation of the alternative complement pathway (AP):
plasma C3, C5, and properdin levels are transiently
decreased in the presence of preserved concentrations of
C4.
6. Current hypotheses:
1. Antibodies bind to streptococcal antigen(s) planted in the
glomerular basement membrane leading to alternative
complement pathway activation.
2. Two streptococcal proteins, have been identified in the
GBM of APSGN patients and proposed as pathogenic
antigens.
3. Antigen-antibody complexes are formed in the circulation
and deposited in the glomeruli and may incite glomerular
damage through activation of the complement system.
7. APIGN due to streptococcal pharyngitis peaks during
winter and early spring
Due to Skin Infection (pyoderma) peaks in late summer
and early fall and the latter is more common in tropical
and subtropical regions.
It occurs at any age but peaks in children ages 6–10 (2–12)
years.
Male to female ratio 2:1.1.
Siblings are also at risk of developing subclinical nephritis.
8. Clinical Features
The clinical manifestations ranges from asymptomatic
microhematuria to severe disease Complications due to
hypertension, renal failure, and cardiac insufficiency.
Hypertension
Edema
Hematuria
Protienuria
Oliguria.
Acute kidney injury.
9. Hypertension (60%)
Headache, vomiting, seizures,
somnolence/altered mental status, Risk of posterior
reversible encephalopathy syndrome (PRES) with visual
changes and focal neurological signs
10. Edema.
Facial/periorbital, dependent, or generalized
edema (more frequently in young children) Ascites, pleural
effusion, Cardiac insufficiency (orthopnea, dyspnea,
cough, pulmonary crackles/edema, and gallop rhythm)
12. Proteinuria.
Mild to moderate, rarely nephrotic range
(>1g/m2/day)
Oliguria.
Transient oliguria in 50 %, complete anuria rare
13. Acute kidney injury.
Nausea, vomiting fatigue, weakness, pallor
Others.
Back pain and abdominal discomfort, fever, weight
gain (edema)
14. Investigations
Urine.
Dipstick analysis
Hematuria, proteinuria
Urine microscopy
Red blood cell (RBC) and mixed cellular casts
Dysmorphic RBCs
Leukocytes (sterile pyuria)
Proteinuria
<2 g/l in 85 % of cases (U protein/creatinine <2 g/g)
Nephrotic presentation may herald poor renal outcome
15. Complement
Reduced plasma C3 and CH50 in >90 % of cases
Normalize within 6–12 weeks after presentation.
Plasma C4 generally normal.
16. Bacterial
Pharyngeal swab
Index patient and siblings (opportunity of
preventing spread of nephritogenic strain)
Culture of beta-hemolytic streptococci
Rapid streptococcal antigen test
Skin swab
Suspected pyoderma
17. Serology.
Antistreptolysin O titer (ASOT);
Elevated in 70–80 % 1–5 weeks after infection, decrease
to preinfection levels after several months.
Unreliable for streptococcal pyoderma or infection by
other organisms
Streptozyme test;
Detecting antibodies against several streptococcal
antigens (streptolysin O, DNaseB, hyaluronidase, streptokinase,
anti-nicotinamide adenine dinucleotidase (NADase)
Anti-Dnase B;
Elevated in 80–90 % of cases of pyoderma-associated
APSGN
18. Kidney biopsy Indications (rare):
Alternative diagnosis (e.g., MPGN, IgA).
Normal serum C3/CH50.
Persistently low serum C3 or CH50 (>12 weeks after
onset).
Persistent GN/deteriorating renal function.
19. Natural resolution.
The acute phase usually lasts 4-10 days when urine output
gradually increases; edema subsides and RFTs return to
normal.
Gross hematuria seldom persists beyond the weeks but
microscopic hematuria may persist for 1-2 years.
Low grade proteinuria may be found up to months after
onset of AGN.
Long-term prognosis is excellent.
The incidence of CKD remains 1% after APSGN
20.
21. General/Supportive treatment
1. Bed rest:
Patient should be preferably hospitalized for close
monitoring of BP and any derangement of RFTs and treatment of any
complications as they arise.
1. Antibiotics:
2. Dietary restrictions:
22. Treatment;
Hypertension and fluid overload;
Restriction of sodium and fluid intake
Loop diuretics (furosemide)
Antihypertensive drugs
If blood pressure is not controlled with
diuretics Preferably calcium channel blocker or angiotensin-
converting enzyme inhibitor (ACEi)
23. Pulmonary edema (rare);
Hypertensive urgency or emergency (with or
without CSN symptoms);
Loop diuretics, Oxygen therapy
Oral agents (nifedipine, hydralazine, minoxidil)
Intravenous agents (nitroprusside, nicardipine,
labetalol)
24. Hyperkalemia;
Loop diuretic
K restriction,
sodium polystyrene sulfonate
Inhaled bronchodilator,
IV calcium or bicarbonate, or insulin drip
If refractory, dialysis
25. Dialysis or continuous veno-venous hemofiltration
Life-threatening hyperkalemia
Severe fluid overload unresponsive to diuretics
Rapidly progressive GN with persistent oligoanuria
26. Antibiotics;
Obtain throat cultures from patient, family members, and
close contacts
Treat those infected to minimize spread of nephrito-
genic strain
Oral penicillin V for 10 days (<25 kg = 250 mg twice
daily, >25 kg 500 mg twice daily)
Erythromycin (40 mg/kg for 10 days) or derivative for
patients allergic to penicillin
27. Prognosis and Outcome;
Short- and long-term prognosis of APSGN in children is excellent.
95 % of the patients recover renal function within 3–4 weeks.
Chronic or progressive kidney disease <1 % of children (higher percentage in
adults).
Recurrence of APSGN extremely rare due to streptococcal type-specific, long-
lasting immunity and limited number of nephritogenic GAS strains.