This presentation discusses about the etiology, clinical features, complications and management of Septic Shock.
The information compiled in this presentation (from medical textbooks and internet sources) does not belong to me, but has been done so for educational purposes
This presentation focuses on the entity known as pyrexia of unknown origin / fever of unknown origin. It demonstrates both common and rare causes, and the epidemiological trend, its clinical presentation, management and prognosis.
This presentation discusses about the etiology, clinical features, complications and management of Septic Shock.
The information compiled in this presentation (from medical textbooks and internet sources) does not belong to me, but has been done so for educational purposes
This presentation focuses on the entity known as pyrexia of unknown origin / fever of unknown origin. It demonstrates both common and rare causes, and the epidemiological trend, its clinical presentation, management and prognosis.
Fever and Hyperthermia and Pyrexia of unknown origin by Dr Mohammad Hussien for Medical Student .
Ass.Lecturer of Hepatogastroentrology at Kafrelsheikh University.
The syndrome of pyrexia of unknown origin (PUO) was first defined in 1961 but remains a clinical challenge for many physicians. Different subgroups with PUO have been suggested, each requiring different investigative strategies: classical, nosocomial, neutropenic, and HIV-related. This could be expanded to include the elderly as a fifth group. The causes are broadly divided into four groups: infective, inflammatory, neoplastic, and miscellaneous. Increasing early use of positron emission tomography–computed tomography (PET-CT) and the development of new molecular and serological tests for infection have improved diagnostic capability, but up to 50% of patients still have no cause found despite adequate investigations. Reassuringly, the cohort of undiagnosed patients has a good prognosis. In this article we review the possible aetiologies of
The definition of pyrexia of unknown origin (PUO) dates back to 1961; it was described as a persistent fever above 38.3°C (100°F) that evades diagnosis for at least 3 weeks, including 1 week of investigation in hospital. PUO and present a systematic clinical approach to the investigation and management of patients, recommending potential second-line investigations when the etiology is unclear
Approach to a patient with fever of unknown origin sunil kumar daha
Please find the power point on Approach to a patient with fever of unknown origin . I tried to present it on understandable way and all the contents are reviewed by experts and from very reliable references. Thank you
Fever and Hyperthermia and Pyrexia of unknown origin by Dr Mohammad Hussien for Medical Student .
Ass.Lecturer of Hepatogastroentrology at Kafrelsheikh University.
The syndrome of pyrexia of unknown origin (PUO) was first defined in 1961 but remains a clinical challenge for many physicians. Different subgroups with PUO have been suggested, each requiring different investigative strategies: classical, nosocomial, neutropenic, and HIV-related. This could be expanded to include the elderly as a fifth group. The causes are broadly divided into four groups: infective, inflammatory, neoplastic, and miscellaneous. Increasing early use of positron emission tomography–computed tomography (PET-CT) and the development of new molecular and serological tests for infection have improved diagnostic capability, but up to 50% of patients still have no cause found despite adequate investigations. Reassuringly, the cohort of undiagnosed patients has a good prognosis. In this article we review the possible aetiologies of
The definition of pyrexia of unknown origin (PUO) dates back to 1961; it was described as a persistent fever above 38.3°C (100°F) that evades diagnosis for at least 3 weeks, including 1 week of investigation in hospital. PUO and present a systematic clinical approach to the investigation and management of patients, recommending potential second-line investigations when the etiology is unclear
Approach to a patient with fever of unknown origin sunil kumar daha
Please find the power point on Approach to a patient with fever of unknown origin . I tried to present it on understandable way and all the contents are reviewed by experts and from very reliable references. Thank you
A brief discussion of a very common bacterial infection presenting as fever and skin rash following skin infection or use of tampons. Affecting adults especially women. Very helpful for medical students, ER doctors, dermatologists, nurses. References from dermatology textbook Rooks.
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.
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Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journey
6 rheumatic fever
1. •
Rheumatic fever
Rheumatism – systemic inflammatory disease of the connective tissue with main localization of the process
in the cardio-vascular system, developing in connection with acute infection (group A beta-hemolytic
streptococсus) in predisposed patients; the peak age-related incidence is between 7 and15 years.
•
Factors of pathogeneсity of Streptococcus
•
М-protein – factor of virulence, has antigenic properties, promotes stability to phagocytosis .
•
Streptolysin - S –exerts direct toxic influence on the erythrocytes, platelets, cells of the myocardium
and kidney by means of increasing permeability of their cellular and lysosomic membranes.
•
Streptolysin О - inducts production of cytotoxic antibodies,
•
Streptohyaluronidase – increases permeability of tissues for the toxines
•
Streptoproteinase – causes destruction of the protein-mucopolysaccharide complex – main
substance of connective tissue.
•
Hyaluronic acid – capsule component, supresses phagocytic activity of neutrophiles.
•
Peculiarities of rheumatism:
1) Connection with acute streptococcal infection;
2) Presence of “absolute signs” of the rheumatism – Jones criteria;
3) Tendency to formation of valvular lesion.
•
The Jones Criteria for Rheumatic Fever, Updated 1992
•
Major Criteria
Carditis
Migratory polyarthritis
•
Sydenham's chorea
•
Subcutaneous nodules
Erythema marginatum
•
Minor criteria
•
Clinical
•
Fever
•
Arthralgia
2. •
Laboratory
•
Elevated acute phase reactants
•
Prolonged PR interval
•
The Jones Criteria for Rheumatic Fever, Updated 1992
•
plus :
•
Supporting evidence of a recent group A streptococcal infection (e.g., positive throat culture or
rapid antigen detection test; and/ or elevated or increasing streptococcal antibody test)
•
Periods of the development of rheumatism
First period
During 2 to 4 weeks after streptococcal infection.
Asymptomatic or with the signs of prolonged recovery.
•
Periods of development of rheumatism
Second period
Clinically evident disease
Development of polyarthritis, carditis, etc.
Clinical, morphologic and immunobiochemical changes, typical for the
primary rheumatism.
•
Periods of development of rheumatism
Third period
Multiform manifestations of the recurrent rheumatism.
Progression of the severity of valvular heart disease.
Development of hemodynamic failure.
•
Diagnosis of rheumatism
•
Primary rheumocarditis (70–85%)
•
Chronological association with А-streptococcal infection (pharyngitis, tonsillitis)
•
Latent period 2 – 4 weeks
3. •
Young age of the patient
•
Mainly acute or subacute onset
•
Polyarthritis or acute arthralgias in the beginning of the disease
•
Presence of valvulitis in connection with myocarditis or pericarditis
•
Quick modification of the symptoms of carditis
•
Correlation of laboratory and clinical data of activity of disease
•
Primary rheumocarditis
Signs of myocarditis
•
•
Cardiomegaly,
•
Weakening of the apex impulse,
•
Cardiac rhythm disturbances (tachycardia, bradycardia, atrial fibrillation)
•
А-V block,
•
Decreased heart sounds,
•
•
Precordial chest pain,
Functional systolic murmur on the apex, not connected with S1
Primary rheumocarditis
ACС Criteria of carditis
(American College of Cardiologists) :
Appearance of new organic or dynamics of previous heart murmurs
Cardiomegaly in the absence of other reasons
Congestive heart failure in young patients in the absence of other reasons
Pericarditis
•
Primary rheumocarditis
ECG peculiarities
•
Prolonged PR interval,
•
Rhythm disturbances:
Extrasystole
Atrial fibrillation
4. •
Disturbances of ventricular repolarization,
•
Prolongation of electric systole (Q-T interval).
•
АV block I degree in patient with acute rheumatic fever
•
EchoCG
•
Thick mitral valve leaflets
•
“Tousled” of the echosignal from the leaflets of the affected valves,
•
Decreased motion of the mitral valve leaflets,
•
Systolic dysfunction of the myocardium.
•
Recurrent rheumocarditis
•
Proceeds with combined valvular heart disease
•
Chronic lingering or latent course.
•
Rheumatic polyarthritis (60-100%)
•
Mainly big and middle joints (knees,elbows,ankles,wrists). Doesn’t affect the small joints of the
hand or feet.
•
benign
•
Short-term
•
migratory
•
Salicylates and other anti-inflammatory drugs usually cause prompt resolution of joint symptoms
(during several days or even hours)
•
Sydenham's chorea
(6-30%)
•
Appears in childhood and juvenile age.
•
Choreic hyperkinesia, most expressed in the muscles of distal parts of extremities and facial mimic
muscles
•
Muscular hypotonia,
•
coordination disorders,
•
Psychical and vegetative disturbances.
•
Duration of the attack of acute rheumatic fever in the form of chorea usually takes from 3 to 6
months.
5. •
Erythema marginatum
(4–17% )
•
Evanescent macular eruption with rounded borders
•
Vary in size.
•
concentrated on the trunk and proximal parts of extremities (but not on the face !).
•
Transitory migrating character
•
No itch or induration
•
Turn pale when pressed.
•
Subcutaneous nodules (1–3 %)
•
Rounded, not mobile, painless formations of different size, are found over extensor surfaces of
joints,
are seen most often in patients with long-standing rheumatic heart disease, and are extremely rare in
patients experiencing an initial attack
•
Quickly appear and disappear.
•
Rheumatic pneumonia
•
Exacerbation of dyspnea,
•
Fever,
•
A lot of rales of different calibres in the absence of dull percussion sound.
•
Chest X-rays – local intensification and deformation of lung markings with multiple small foci of
consolidation.
•
Anti-inflammatory treatment leads to prompt normalization of clinical and roentgenologic changes.
•
Rheumatic pleuritis
•
Pleuritic chest pain, exacerbated by breathing and coughing.
•
Pleural rub
•
Fever.
•
Anti-inflammatory drugs cause prompt resolution of the symptoms.
•
Additional manifestations:
GENERAL:
6. •
Fever
•
Adynamia, fatigue, asthenia
•
Paleness
•
Sweating
•
Nasal bleeding
•
Abdominal syndrom
•
Abdominal syndrom
•
Mainly in childhood, in acute course of primary or recurrent rheumatism.
Clinical symptoms:
•
Diffuse or localized pain in the abdomen,
•
nausea, vomiting,
•
Constipation or diarrhea.
•
Additional manifestations
Special:
•
Leucocytosis (neutrophilia)
•
Increasing of erythrocyte sedimentation rate (ESR)
•
hyperfibrinogenemia
•
positive С-reactive protein
•
Increasing of a2- and g- globulins
•
Increasing of serum mucoproteins, glycoproteins
•
Pathologic serologic indices: streptococcal antigen, increased titers
of АSL-О, АSС, АSH.
•
Increased capillary permeability
•
Degrees of activity of rheumatic process
•
Peculiarities of the course:
Acute rheumatic fever – duration of the attack to 3 months, proceeds rapidly, symptoms are evidently
progressing, high titers of antistreptococcal antibodies, prevalence of hypersensitivity of immediate type
reactions (desorganisation of connective tissue and exudative cell reactions).
7. •
Peculiarities of the course:
Subacute rheumatism – duration of the attack from 3 to 6 months, proceeds rapidly, symptoms are
progressing, high titers of antistreptococcal antibodies, prevalence of hypersensitivity of immediate type
reactions (desorganisation of connective tissue and exudative cell reactions).
•
Peculiarities of the course:
Lingering illness– with the constant development of symptoms and I –II degree activity more than 6
months,without clear remissions and weak, unstable effect of anti-inflammatory treatment .
•
Peculiarities of the course:
Persistently-recurrent – undulating with с exacerbations and incomplete remissions, with I – III degree
activity up to 1 year and more.
•
Peculiarities of the course:
Latent course – can’t find a disease, which may be considered as missed rheumatic attack; can’t reveal even
minimal activity of pathologic process, but clinically certain acquired valvular heart disease is estalished.
•
Plan of laboratory and instrumental examination:
•
CBC (complete blood count)
•
Thermometry during 2 hours
•
Protein fractions
•
С-reactive proteine (CRP)
•
Titers of anti-streptolysin O, anti-streptohyaluronidase and anti-deoxyribonuclease B
•
ECG
•
PhonoCG, EchoCG, Doppler-EchoCG.
•
Classification of Nesterov A. (1964)
•
TREATMENT
•
There are two necessary therapeutic approaches to patients with acute rheumatic fever: antistreptococcal antibiotic therapy and therapy for the clinical manifestations of the disease
•
Etiotropic treatment
•
Goal: eradication of group A b-hemolytic Streptococcus.
•
Benzylpenicillin in daily dose 1 500 000 – 4 000 000 units in adults and teenagers and 400 000 – 600
000 units in children for 10-14 days course.
8. •
Following transition to retard form of penicillin (benzathine penicillin).
•
Pathogenetic treatment
Nonsteroidal antiinflammatory drugs (NSAIDs).
•
Pathogenetic treatment
Glucocorticosteroids.
•
Prednisolon 20 – 30 mg/day up to 2 weeks with following tapering (2,5 mg every 5 – 7 days) till the
complete cancellation.
•
Triamcinolon 12 – 16 mg/day
•
Primary prophylaxis
•
Proper time diagnosis of А – streptococcal infection of pharynx and tonsils.
•
Conventional antibiotic treatment should be started immediately: a complete 10-day course in
adults of either oral penicillin V (500 mg twice daily), or erythromycin (250 mg four times daily) for
those with penicillin allergy.
•
In chronic recurrent streptococcal tonsillopharyngitis:
•
macrolides,
•
oral cephalosporines.
•
But no one above-mentioned medication (or their combination )doesn’t guarantee 100%
elimination of the streptococcus from nasopharynx.
•
Secondary prophylaxis
•
Prevention of recurrent attacks and progress of the disease in patients after acute rheumatic fever.
•
Regular infusion of prolonged penicillin (benzathine penicillin )
•
Insufficient efficacy of bicillinoprophylaxis in 13 – 37 % of patients.
•
Secondary prophylaxis
•
Benzathine penicillin G–2,4 million units intramuscular every 3 weeks
•
Since it is known that the risk of recurrence of rheumatic fever is highest during the first 5 years
after the attack, secondary prophylaxis is always given for at least this period.
•
After that the decision to continue or discontinue secondary prophylaxis is dependent upon
whether the patient has documented rheumatic heart disease and whether the patient is at high
risk of exposure to streptococci (e.g., students, school teachers, medical and military personnel,
etc.). Many believe that those with documented recurrences and/or documented rheumatic
9. valvular heart disease should receive secondary prophylaxis for life. The duration of prophylaxis is
often individualized for specific patients.