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Asthma : types, pathophysiology, diagnosis and treatment

 Bronchial asthma Asthma is a chronic inflammatory disease of the smaller airways, characterised by episodic, reversible bronchial obstruction due to hyper-responsiveness of tracheobronchial tree to a multiplicity of intrinsic and extrinsic stimuli manifested clinically by paroxysms of polyphonic wheeze, dyspnoea, chest tightness and cough which may be relieved spontaneously or as a result of therapy. ASTHMA BRONCHIOLE Types of Asthma Extrinsic Asthma (Atopic Asthma, Early Onset Asthma) Onset is in childhood. It occurs in atopic individuals who readily form IgE antibodies in response to allergens. Atopic patients can be identified by skin sensitivity tests. Intrinsic Asthma (Non-atopic Asthma, Late Onset Asthma) It can be begin at any age, especially in late adulthood. There is no role for allergens in the production of disease. Nocturnal Asthma It is defined as an overnight fall of more than 20% in the FEV1 or PEFR. This is presumed to be due to: Early morning fall in circulating adre
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Mechanism of Normal Labor

  Mechanism of normal labor Definition: The series of movements that occur on the head in the process of adaptation during its journey through the pelvis is called mechanism of labor. Mechanism:   In normal labor, the head enters the brim more commonly through the available transverse diameter (70%) and to the lesser extent through one of the oblique diameters. The position is either occipitolateral or oblique occipitoanterior. Left occipitoanterior is more common than right occipitoanterior as the left oblique diameter is encroached by the rectum. The engaging anteroposterior diameter of the head is either suboccipitobregmatic 9.5 cm or in slight deflexion-the suboccipitofrontal 10 cm. The engaging transverse diameter is biparietal 9.5 cm. As the occipitolateral position is most common, the mechanism of the labor in such position will be described. The principal movements are: Engagement Descent Flexion Internal rotation  Crowning Extension Restitution External rotation Expulsion of

PLEURAL EFFUSION

  Pleural Effusion: Causes, Clinical features, Investigations And Management Pleural effusion is the accumulation of serous fluid in the pleural cavity. Mechanism of Pleural Fluid Formation Elevation of venous pressure (rare in pure Right Ventricular failure) Decreased plasma oncotic pressure (except in congenital hypoalbuminuaemia) Increased capillary permiability due to local inflammation, toxins or vasoactive substances as occurs in collagen-vascular diseases, pancreatitis, pulmonary emboli and pneumonitis Increase in pleural space oncotic pressure as a result of : Protein leak through capillaries, Protein exudation due to local pleural inflammation, Defective lymphatic absorption. Simple transfer of ascitic fluid across diaphragmatic defect and also through transdiaphragmatic lymphatics as occurs in cirrhosis and Meig's syndrome. Increased negativity of pressure in the pleural also results in pleural effusion as occurs in atelectasis. Obstruction of lymphatics. Pleural fluid, o

ACNE VULGARIS

  Acne vulgaris Acne vulgaris is a disorder of pilosebaceous complex which predominantly affects the peripubertal population and clinically manifests as comedones (open- blackheads, closed- whiteheads), papules, nodules, pustules and cysts and heals with scars. Pathogenesis 1. Occlusion of pilosebaceous orifice Pilosebaceous orifice in acne is occluded by a keratinous plug induced by: chemicals (cosmetics) and reduced levels of linoleic acid in sebum of acne patients. Results in retention of sebum, encouraging growth of microbes, triggering a vicious cycle. Distended follicle ruptures, releasing proinflammatory chemicals into the dermis, stimulating intense inflammation.  Ductal epithelium also produces cytokines and an inflammatory cascade is triggered. 2.  Increased sebum production Sebaceous gland activity is controlled by androgens. Most patients have normal levels of circulating androgens, but their sebaceous glands are unusually sensitive to androgens due to an enhanced end organ

Alopecia (Baldness)

 Alopecia: causes, diagnose, and treatment Alopecia : Alopecia means loss of hair. There are two types of alopecia. Non-cicatricial alopecia Cicatricial alopecia Difference between cicatricial and noncicatricial alopecia Alopecia Areata (AA) Etiology The pathogenesis of AA is uncertain and following factors are incriminated: Immunological factors: AA is considered an immunological disease because of: Association of AA with other auto-immune diseases (auto-immune thyroid disease, pernicious anemia, vitiligo, and atopy) Cytokines produced by dermal papillae in lesions not only attract lymphocytes to perifollicular region but also stimulate them to multiply. As opposed to normal hairs, strong major histocompatibility complex (class 1 and class 2) immunoreactivity found in affected follicles. 2. Genetic factors: AA may be present in some families, so it may have a genetic basis. 3. Emotional factors: In some patients, AA is precipitated by emotional stress. Epidemiology     Prevalence:   A

Rheumatoid arthritis (RA)

  Rheumatoid arthritis  is a chronic inflammatory, destructive and deforming symmetrical polyarthritis associated with systemic involvement. The individuals with HLA-D4 and HLA-DR4 are more prone to RA. It starts when your immune system, which is supposed to protect you, goes awry and begins to attack your body’s own tissues. It causes  inflammation   in the lining of your joints (the synovium). As a result, your joints may get red, warm, swollen, and painful. Symptoms of Rheumatoid Arthritis Joint pain and swelling Stiffness, especially in the morning or after you sit for a long time Fatigue Who Gets Rheumatoid Arthritis? Anyone can get RA. It affects about 1% of Americans. The disease is 2 to 3 times more common in women than in men, but men tend to have more severe symptoms. It usually starts in middle age. But young children and the elderly also can get it. Pathogenesis Synovitis (synovial cell hyperplasia, hypertrophy with CD4 lymphocytic infiltration and synovial effusion) Pannus