Pathogenesis of Hepatitis B

Eradication of HBV infection depends on the coordinate and efficient development of humoral and cell-mediated immune responses against HBV proteins. Antibodies secreted by plasma cells (PC) derived from antigen-specific B cells (which usually recognize viral antigens in their native conformation) are mostly responsible for the neutralization of free circulating viral particles, Cytotoxic T cells (CTL) that recognize endogenous viral antigens in the form of short peptides associated with human leukocyte antigen (HLA) class I molecules on the surface of the infected hepatocytes (HC) are the main effectors for the elimination of intracellular virus. They can do this by at least two different mechanisms: direct attachment to the cell membrane, causing the infected cell to undergo apoptosis; and the release of soluble cytokines that can downregulate viral gene expression, leading to the elimination of intracellular virus without destruction of the infected cell. Both humoral and cytotoxic functions are more or less stringently regulated by the helper effect of the CD4+ T cells (TH) that recognize exogenous viral antigens, released or secreted by liver cells, in the form of short peptides that associate with HLA class II molecules in the endosomal compartment of professional antigen-presenting cells such as B cells, macrophages (Mø), and dendritic cells.

THE ABC OF STROKE MANAGEMENT

 

ACUTE STROKE

A: Airway

B: Breathing

C: Cardio-respiratory

D: Drugs

E:  Electrolyte

F:  Fluids

G:  Glucose

H:  Hydration

I :  Intake/nutrition : dysphagia à enteral/parenteral nutrition

                                caloric/nutrients/vitamins/trace elements

REHABILITATION: as soon as the condition of patient is stable

 

IMPORTANT THINGS TO BE KEPT IN MIND:

•         STROKE  is first of all a vascular event.It is and should be treated as a part of systemic(vascular) diseases

•         The already infarcted brain tissue can not regenerate.The only left for intervention is the penumbra/ischemic area,which treatment depend on the normalization  of the risk factor influencing (systemic) vascular con- dition

•         Up to the moment the what so called “neuro protective agents” has no evidence  proved  benefits (Penhall,2001)

•         Rehabilitation measures seem to be beneficial due to the brain plasticity

 

Viral Infections of Adenotonsil

Patients presenting with viral tonsillitis, usually simultaneously with viral pharyngitis, commonly complain of sore throat and difficulty swallowing. Upon examination, there is often fever and oropharyngeal erythema, usually without a tonsillar exudate. Viruses such as adenovirus, rhinovirus, reovirus, respiratory syncytial virus (RSV), and the influenza and parainfluenza viruses have all been shown to be possible pathogens. Most of these infections are self-limited and require only symptomatic treatment.

The Epstein-Barr virus (EBV) causes acute pharyngitis as a part of infectious mononucleosis syndrome. It is common in children and young adults, is transmitted by oral contact, and manifests as fever, generalized malaise, lymphadenopathy, hepatosplenomegaly, and pharyngitis. Upon examination, petechiae may be present at the junction of the soft and hard palates. The tonsils are severely enlarged, sometimes to the point of compromising the airway, and classically are covered with an extensive grayish-white exudate. A complete blood count (cbc) may be significant for lymphocytosis with atypical lymphocytes (activated T-cells). A Monospot test is more sensitive and specific than a heterophil antibody test, which can be negative in 10–15% of patients in the first week of illness. Treatment is largely supportive, with IV fluids and rest. In the case of progressive airway obstruction due to obstructive tonsillar swelling, a short course of systemic steroids can be very helpful. Rarely, a nasopharyngeal airway, nasotracheal intubation, or tracheotomy may be required to secure the airway.

Tonsillar infections with the Coxsackie virus result in herpangina, which presents as ulcerative vesicles over the tonsils, posterior pharynx, and palate. The disease commonly occurs in children under the age of 16. Patients present with generalized symptoms of headache, high fever, anorexia, and odynophagia.

Treatment for viral infections is mostly supportive, but the tonsils can have a bacterial superinfection that results in more severe symptoms. These patients can benefit from systemic antibiotics.

Acute Otitis Media

Essentials of Diagnosis

• Otalgia.
  
• Pyrexia.
  
• Thickened, bulging, hyperemic tympanic membrane.
  
• Hearing loss.
  
• ± Otorrhea.
  

Symptoms and Signs

Prior to the onset of symptoms of AOM, the patient frequently has symptoms of an upper respiratory tract infection. Older children will usually complain of earache, whereas infants become irritable and pull at the affected ear. A high fever is often present and may be associated with systemic symptoms of infection, such as anorexia, vomiting, and diarrhea. Otoscopy classically shows a thickened hyperemic tympanic membrane, which is immobile on pneumatic otoscopy.

Further progression of the infective process may lead to the spontaneous rupture of the tympanic membrane, resulting in otorrhea. If this occurs, the otalgia and fever often subside. At this stage, it is often not possible to visualize the tympanic membrane due to the discharge in the ear canal.

Otitis Media with Effusion

Otitis media with effusion may be completely asymptomatic and only detected on routine audiologic screening. The most common symptom of OME is hearing loss. While older children may complain of reduced hearing, in many cases the hearing loss is noticed by parents, a nursery nurse, or a teacher. In younger children, the only symptom may be delayed speech development or behavioral problems. Another common symptom is a "blocked" feeling in the ear, which may cause infants and young children to pull at their ears. More rarely, symptoms of earache, tinnitus, or balance disorder may be present.

Otoscopy classically reveals a dull gray- or yellow-colored tympanic membrane that has reduced mobility on pneumatic otoscopy. If the tympanic membrane is translucent, an air-fluid level or small air bubbles within the middle ear effusion may be seen

Pathogenesis of Sinusitis

The anatomy of the sinuses does not promote passive gravitational drainage and therefore the cilia of the sinonasal mucosa must function properly. Without the constant movement of mucus from the sinuses into the nose, accumulation and eventual infection is inevitable. This fact is illustrated by disorders such as Kartagener syndrome, in which ciliary movement is abnormal.

The cilia of the maxillary sinus propel mucous toward the natural ostia of the sinus, explaining why large openings made into the maxillary antrum at places other than the natural ostia (eg, in the inferior meatus) are ineffective at draining the sinus.

Acute sinusitis may begin with edema of the nasal mucosa and the resultant blockage of the sinus ostia, which then results in stasis and infection. The most common organisms responsible for acute sinusitis include Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis. Depending on the geographic location, approximately one third of S. pneumoniae isolates are resistant to penicillin and one third of H. influenzae produce -lactamase. Nearly all isolates of M. catarrhalis produce -lactamase.

Chronic sinusitis arises from longstanding inflammation of the sinonasal mucosa and is often caused by bacteria different from the bacteria that produce acute sinusitis. Laboratory studies in which maxillary mucopus was cultured during endoscopic surgery showed a high percentage of coagulase-negative Staphylococci, Staphylococcus aureus, and Streptococcus viridans.

Corynebacterium and anaerobes were also isolated. Although coagulase-negative Staphylococcus is often considered a contaminant, the organism may have a pathologic role in chronic sinusitis. Also of note, the coagulase-negative Staphylococcus isolated displayed significant antimicrobial resistance. In other studies of chronic sinusitis bacteriology, a similar range of organisms was cultured except that Pseudomonas was identified in a significant number of the isolates. One half of these Pseudomonas isolates were resistant to quinolones.

Fungus may also infect the paranasal sinuses, causing a wide range of disease. Certain species, specifically Mucor, cause invasive fungal sinusitis. Invasive fungal sinusitis is typically seen in the diabetic or immunocompromised patient and is characterized by a rapidly progressive course. The skull base and orbit are frequently involved, necessitating aggressive surgical and medical management. Fungus can also stimulate an immune response from the sinonasal mucosa, resulting in allergic fungal sinusitis. Typically, polypoid tissue is seen anterior to a mass consisting of mucin, fungal elements, Charcot-Leyden crystals, and eosinophils. Sinus expansion and bony remodeling are hallmark features of this process. Even though this is not an invasive, infectious process, the treatment is surgery with immunotherapy as a critical adjunct.