Three main factors contribute to this: peribronchial fibrosis, build-up of scar tissue from damage to the airways and over-multiplication of the epithelial cells lining the airways.3,4 Parenchymal destruction is associated with loss of lung tissue elasticity, which occurs as a result of destruction of the structures supporting and feeding the alveoli (emphysema). This means that the small airways collapse during exhalation, impeding airflow, trapping air in the lungs and reducing lung capacity (Figure 2). Inflammatory cells__2 Figure 1: Inflammatory and immune cells involved in COPD.2 Adapted from Barnes, PJ. Nat Rev Immunol 2008;8:183-92 11grafik2 Figure 2: Airflow limitation in
Acute inflammation is a rapid response to an injurious agent that serves to deliver mediators of host defense—leukocytes and plasma proteins—to the site of injury. Acute inflammation has three major components: alterations in vascular caliber that lead to an increase in blood flow; structural changes in the microvasculature that permit plasma proteins and leukocytes to leave the circulation; and emigration of the leukocytes from the microcirculation, their accumulation in the focus of injury, and their activation to eliminate the offending
B -Environmental Lung Diseases: *Result from inhaled dust or chemicals *Pneumoconiosis is a general term used for a group of lung diseases caused by inhalation and retention of mineral, metal or dust particles *Repeated exposure to the irritant can cause pul. Fibrosis -Chemical pneumonitis *Results from exposure to toxic chemicals *Clinically pt has pul edema -Hypersensitivity pneumonitis *An individual inhales irritants to which they are allergic too *Clinical manifestations occur w/in 4-6 hrs of exposure and incl. fever, chills, cough, SOB and malaise Clinical Manifestations: -Typically do not appear for 10-15 yrs after exposure but incl. dyspnea, coughing, wheezing and weight loss -Cor pulmonale is a late manifestation. *Cor pulmonale is an enlargement of the right ventricle Check what ya know (Answers at end) 6.)
The acute phase response develops in a wide range of acute and chronic inflammatory conditions like bacterial, viral, or fungal infections; rheumatic and other inflammatory diseases; malignancy; and tissue injury or necrosis. These conditions cause release of interleukin-6 and other cytokines that trigger the synthesis of CRP and fibrinogen by the liver. During the acute phase response, levels of CRP rapidly increase within 2 hours of acute insult, reaching a peak at 48 hours. With resolution of the acute phase response, CRP declines with a relatively short half-life of 18 hours. Measuring CRP level is a screen for infectious and inflammatory diseases.
In cutaneous anthrax there is a 1 to 7 day of incubation period, a small papule appears at the site of inoculation. A papule is a small solid pimple or swelling that may form a rash and may typically be inflamed. It develops into a vesicle filled with clear fluid. Subsequently, a small ring surrounding of similar vesicles develops and fuses. This fusion turns into a large lesion causing erythema, which is superficial reddening of the skin, pruritis a severe itching of the skin and non pitting edema ( swelling in certain parts of the body) pain is rarely experienced.
Clostridium Difficile Clostridium Difficile, often called C. difficile or C. diff, is a bacterium that can cause Symptoms ranging from diarrhea to life - threatening inflammation of the colon. Illness from C. difficile most commonly affects older adults in hospitals or in long term care facilities and typically occurs after use of antibiotic medications. In recent years, C. difficile infections have become more frequent, more severe and more difficult to treat. Each year, tens of thousands of people in the United States get sick from C. difficile, including some otherwise healthy people who aren’t hospitalized or taking antibiotics.
What is a sickle cell crisis? Why is it concerning? • A sickle cell crisis is when the RBC is sickled shaped which prevents the RBC’s and oxygen to get to the tissue leading to extreme pain. There are 3 forms of a sickle cell crisis: • Vaso-occlusive crisis occurs when blood flow to tissues is obstructed by sickled RBCs, leading to hypoxemia and ischemia. • Acute sequestration event occurs when blood flow from an organ such as the liver, lungs, or spleen is obstructed by sickled RBC.
Invades nasopharynx where it replicates & spreads down to lower airway via aspiration of upper airway secretions. Causes necrosis of respiratory epithelium of small airways, peribronchiolar mononuclear infiltration & plugging of the lumens with mucus and exudate. The small airways become variably obstructed; this allows adequate inspiratory volume but prevents full expiration. This leads to hyperinflation & atelectasis. Serious alterations in gas exchange occur with arterial hypoxemia & CO2 retention resulting from mismatching of pulmonary ventilation (gas exchange w/in lungs) and perfusion.
Multiple Sclerosis is provoked by damage to the myelin sheath which is the protective covering that surrounds the nerve cells. When the sheath is damaged the nerve impulses may slow down or even stop. Inflammation is what causes the nerve damage. When the nervous system is attacked by its own immune cells, inflammation occurs. Repeated inflammation can occur along any area of the brain, spinal cord, or the optic nerve (PubMed Health 1747) (PubMed Health 1463).
An ischemic stroke is usually characterized by a reduction or obstruction of blood supply to the brain due to blocked blood vessels caused by atherosclerosis or a blood clot. Up to twelve percent of ischemic strokes often cause death within thirty days and is among the largest health burdens in developed countries. It is worth noting that the epidemiology of stroke has been changing because of several factors, with the most important being an ageing population, as well as advancements in the treatment of the condition. Stroke prevalence is projected to increase globally as the population of individuals aged above sixty-five years augments (Ovbiagele et al., 2013, p. 2363). Ovbiagele et al.