Sore throat

"Sore throat” or pharyngitis is one of the most frequent complaints of patients in the acute care setting. On the surface, pharyngitis would appear to pose few challenges to the clinician; the site of infection is both visible and accessible for inspection and culture, and the majority of pharyngeal pathogens are self-limiting respiratory viruses. Unfortunately, the diagnosis and management of acute pharyngitis is complicated by the 10% to 30% of cases caused by bacterial pathogens, particularly group A beta-hemolytic streptococci (GAS). Concerns over the risk of suppurative and nonsuppurative complications associated with GAS pharyngitis have fueled the widespread practice of empirical antimicrobial?therapy. However, the consequences of antimicrobial overuse, measured by cost, adverse events, and bacterial resistance, have refocused attention on the need for targeted therapy based on an appreciation of the epidemiology and diverse clinical presentations of acute pharyngitis.


Clinical Manifestations
The principal challenge IS TO MAKE DIFFIRENCE  BETWEN viral AND bacterial causes, Pharyngitis IS defied as mucous membrane inflmmation either

localized to the posterior pharynx or contiguous with the adjacent membranes of the posterior nares or larynx. 

How endocarditis takes place ? (PATHOGENESIS)

The pathogenesis of endocarditis starts with an area of endocardial injury leading to platelet-firin deposition. The next step requires a microorganism to enter the bloodstream and adhere to the area of injury. Injury and infection most commonly occur on the valve leaflts but can also occur on or near congenital defects, chordae, chamber walls, prosthetic valve attachments, pacemaker leads, or any other endocardial location where conditions are met. Subacute bacterial endocarditis most commonly occurs on the downstream side of a signifiant pressure gradient related to the rheumatic heart lesions, bicuspid aortic valve, or a variety of congenital heart lesions such as ventricular septal defect. Predisposing factors select organisms to enter the blood stream, and once present, adherence factors determine the like lihood of a particular organism causing endocarditis. Adherence facilitates the initial colonization of the valve surface. Certain species of bacteria—for example, Staphylococcus and Streptococcus species—produce the majority of the human cases of endocarditis because of their ability to adhere to damaged tissues of the heart. Conversely, Escherichia coli can be a common cause of bacteremia from urinary or gastrointestinal sources but is a rare cause of endocarditis because it lacks these adherence factors.


In 1978 Drs. Sheld, Valone, and Sande described the role of dextran, platelets, and fibrin in the adherence of streptococci to damaged endocardial tissue. Staphylococci use a variety of surface-bound adhesion components to bind to firinogen for colonization and fironectin for invasion. Certain enzyme possess clumping factor binding firinogen and fironectin as a virulence factor. Once attached to the platelet-firin nidus, bacteria begin to multiply, increasing coagulation activation, attraction of leukocytes, and growth of inflmmation-promoting vegetation This in effect buries bacteria deep within the mature vegetation, contributing to the treatment challenge of IE.

Acute appendicitis

Acute appendicitis is the most common surgical emergency, and appendectomy is the most common emergency operation, with more than 250,000 procedures reported annually in the United States. Acute appendicitis results from appendiceal endoluminal obstruction, typically caused by a fecalith. Although no specifi risk factors have been identifid, it is slightly more common in males and in the young and the elderly, with more advanced disease on presentation in the elderly. Clinical fidings in combination with basic laboratory tests are often enough to establish
the diagnosis, and imaging studies, such as abdominal ultrasound or computed tomography (CT), can be helpful to confim the diagnosis and rule out other potential pathologies in selected individuals. The treatment for acute appendicitis is appendectomy, and the laparoscopic approach is preferred, given its association with better postoperative outcomes. In later stages, appendicitis may be complicated with phlegmon or intraabdominal abscess. For these patients, aggressive medical treatment with broad-spectrum antibiotics and percutaneous drainage when indicated is the initial treatment of choice, and the operative approach is reserved for when this treatment fails and in the setting of peritonitis. Interval appendectomy after an episode of appendicitis treated with antibiotics, although still controversial, must be considered to minimize the risk of recurrent inflmmation, which is associated with worse outcomes.
Good outcomes are generally seen in patients diagnosed and treated early, and this should be the main goal when approaching patients with suspected acute appendicitis.

Cardiac cell membrane VS The current of activation and ECG presentation

As you can see the negative ions migrate to the outer surface of the cell and the positively charged
ions pass into the cell; this reversal of polarity is called depolarization phase 1
This traffic ions determine the Potential of charges :
So the difference of electrical charge not equal  
i will develop this in the future posts :)

What to do in Shock (circulatory)?

■ Hospitalization in intensive care or intensive care unit USIC.
• optimal oxygenation (O2, VNI, intubation, mechanical ventilation).
• Monitoring ECG, blood pressure, saturation, bloody blood pressure. 
■ First Routes veineux.Types treatment
Cardiogenic shock: dobutamine, diuretic IV, specific treatment
Hypovolemic shock :Fluid replacement by crystalloid or colloid solutions, blood transfusion, the treatment purpose is to increase blood volume Fluid replacement septic shock,
-dopamine, 
-dobutamine,
-norepinephrine
, antibiotic therapy in septic shock, corticosteroids adrenal insufficiency, treating the cause,
 hémofitration continuous high speed,
 activated protein C (CRP)
Fluid replacement anaphylactic shock, epinephrine, corticosteroids

Fibroblast and allergy

Fibroblasts proliferate in response to several cytokines and mediators generated during an allergic inflmmatory response. Recognized firoblast mitogens include histamine, heparin, and tryptase derived from mast cells, and major basic protein (MBP) and eosinophil cationic protein (ECP) from eosinophils. The cytokines TGF- β as well as platelet-derived growth factor (PDGF), b-firoblastgrowth factor (b-FGF), insulin-like growth factor 1 (IGF1), IL-1, and endothelin released during chronic allergic inflmmation promote fibroblast proliferation, differetiation, and activation.TGF-β enhances production of a range of extracellular matrix components, and decreases the synthesis of matrix-degrading enzymes while increasing the synthesis of protease inhibitors. Thus, TGF- β promotes the deposition of extracellular matrix while inhibiting its degradation, and contributes to the widespread subepithelial extracellular matrix deposition that may be associated with chronic allergic inflmmation.Chronic allergic inflmmation may lead to the deposition of types III and V ‘repair’ collagens in the lamina reticularis beneath the types IV and VII ‘reticular’ collagens, which largely make up the basement membrane.The altered sub-basement membrane region also contains increased deposition of extracellular matrix components including fironectin, tenascin, and lamin. Myofiroblasts present below the basement membrane are increased in number in asthma and are the source of many of the extracellular matrix products that are expressed after allergen challenge. so as you see the allergy is phenomenon complex ...

Asthma vs genetics

Now we will talk about asthma and one of the very important question the genetic side of this disease as you know, The dawn of the new century has seen a revolution in our understanding of the
genetic basis of common diseases such as obesity, diabetes, heart disease,
cancer - pathogenenetics -, and neuropsychiatric conditions. These diseases are termed ‘complex
genetic diseases’ as they result from the effect of multiple genetic and interacting environmental factors Like these other common conditions, the role of a heritable component to susceptibility to allergic disease has long been recognized, with atopy and the clinical manifestation of allergy such as asthma and atopic dermatitis resulting from the interaction between an individual’s genetic make-up and their environmental exposures. Recent years have seen considerable progress in unravelling the contribution of specific genetic factors to an individual’s susceptibility, subsequent development, and severity of allergic disease. This has resulted in increasing insight into novel areas of allergic disease pathophysiology. Furthermore, studies of gene–environment interaction have lead to greater insight into the importance of environmental triggers for the initiation, exacerbation, and persistence of allergic diseases. i will develop this soon