Tissue destruction

Frequently, the EAR is followed by a late phase response 4-6 h later and it is caused by the pulmonary sequestration of eosinophils, neutrophils, mast cells, and T-lymphocytes. This leukocyte recruitment depends on mast cell-derived mediators such as TNFa and various chemokines, as well as on the expression of adhesion molecules on leukocytes (e.g. VLA-4, CD11/18) and vascular endothelial cells (e.g. VCAM-1, ICAM-1, E-selectin). Products of these leukocytes have several functions First, they cause the second phase of bron-choconstriction, mucus secretion, and airway swelling second, they cause tissue destruction third, they launch and entertain the chronic inflammation. 

Subchondral bone undergoes metabolic changes, including increased bone turnover, that appear to be precursors to tissue destruction. The normally contiguous bony surface becomes fissured. Persistent use of the joint eventually results in loss of cartilage, permitting bone-to-bone contact that ultimately promotes thickening and eburnation of exposed bone. Microfractures may appear in subchondral bone, and osteonecrosis may develop beneath the surface. 

Approximately two-thirds of all pressure sores occur on the sacrum and heels. The remaining third occur predominately on the elbows, ankles, trochanters, ischia, knees, scapulas, shoulders, or occiput.35 Pressure sores are classified according to the extent of tissue destruction.40 The staging of pressure sores is presented in Table 70-7. 

Imaging studies, such as CT, MRI, or bone scan, can be used to detect osteomyelitis and to determine the depth and extent of tissue destruction. 

Extravasation generally is defined as leakage of intravenous fluids into the interstitial tissue. It is one of the most feared complications of the administration of cytotoxic chemotherapy. While extravasation does not cause death, significant morbidity may result from local tissue destruction, and immediate management is necessary. 

CX is an urticant, producing instant, almost intolerable pain and local tissue destruction immediately on contact with skin and mucous membranes. It is toxic through inhalation, skin and eye exposure, and ingestion. Its rate of detoxification in the body is unknown. 

Whilst the expulsion of intestinal nematodes is absolutely Th2-mediated (Chapter 17 and below), the associated enteropathy is indistinguishable from that previously attributed to Thl-like responses. The solution to this paradox, which is addressed below, may therefore reside in the recognition of common mediators of tissue destruction, remodelling and repair, induced by both Thl and Th2 cytokine-dependent processes. 

May cause severe and painful irritation of the eyes, nose, throat, and lungs. Severe exposure can cause accumulation of fluid in the lungs (pulmonary edema). Inhalation toxicity similar to hydrogen chloride and hydrogen fluoride. May cause second or third degree burns upon short contact with skin surfaces. Oral ingestion may result in tissue destruction of the gastrointestinal tract. Decreased blood cholinesterase levels have been reported in animals. 

Water-miscible solvents alone can be used when the drug is chemically unstable in the presence of any water. The number of solvents available for this purpose is extremely limited. The classic review of this subject was made in 1963 (Spiegel and Noseworthy), and some 30 years later, no additional solvents are available. This is unlikely to change in the near future due to the extensive effort necessary to determine the safety of a solvent used as a vehicle. When a nonaqueous vehicle is used, one can invariably expect some degree of pain upon injection, and subsequent tissue destruction is possible. This damage may be due to the heat of solution as vehicle mixes with body fluids it may be associated with tissues rejecting the solvent or, it may be an inherent property of the solvent. 

Necrosis Actual tissue destruction, masses of dead/destroyed tissue. 

When activated, the instrument delivers a sustained high-frequency AC waveform. Current density is high at the implement and local heating causes tissue destruction. The sine wave continues until the switch is released. 

The prototype of a small pore-forming toxin is the S. aureus a-toxin, also called ct-hemolysin, that has been extensively investigated hy Bhakdi and coworkers. Monomers of ct-hemolysin (33 kDa) hind to the surface of erythrocytes, and after lateral diffusion within the lipid hilayer, seven monomers oligomerize to form pores in the cell membrane. The ct-hemolysin forms mushroom-shaped pores with an outer diameter of lOnm and an inner diameter of approximately 2.5 nm. Small molecules can pass through the pore and diffuse into/out of the cytosol, along with water. As a consequence of such movement, cell homeostasis is greatly disturbed and pushed into an unhealthy state. In animals, the a-hemolysin represents a major virulence factor of S. aureus which causes hemolysis as well as tissue destruction. ... 

There are no reports of adverse effects in humans. By analogy to NaOH, the effects from dust or mist could be expected to vary from mild irritation of the upper respiratory tract to pneumonitis, depending on the severity of the exposure. The greatest industrial hazard is rapid tissue destruction of the eyes on contact with the solid or a concentrated solution. If cesium hydroxide is not removed from the skin, it is anticipated that burns will occur after a period of time. Ingestion would be expected to cause corrosion of the lips, mouth, tongue, and pharynx, as well as abdominal pain. 

HF solutions in contact with skin result in marked tissue destruction undissociated FIF readily penetrates skin and deep tissue, where the corrosive fluoride ion can cause necrosis of soft tissues and decalcification of bone the destruction produced is excruciatingly painful.Fluoride ion also attacks enzymes (e.g., of glycolysis) and cell membranes. The process of tissue destruction and neutralization of the hydrofluoric acid is prolonged for days, unlike other acids, which are rapidly neutral-ized. ° Because of the insidious manner of penetration, a relatively mild or minor exposure can cause a serious burn. When skin contact is with solutions of less than 20%, the burn manifests itself by pain and erythema with a... 

The effects of potassium hydroxide are similar to those of other strong alkalies such as sodium hydroxide. The greatest industrial hazard is rapid tissue destruction of eyes or skin on contact either with the solid or with concentrated solutions. Contact with the eyes causes disintegration and sloughing of conjunctival and corneal epithelium, corneal opacification, marked edema, and ulceration. After 7-13 days, either gradual recovery begins or there is progression of ulceration and corneal opacification, which may become permanent. If potassium hydroxide is not removed from the skin, severe burns with deep ulceration will occur. 

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