- Physical agents.
- Chemical injury.
- Infectious agents.
- Genetic defects.
No category found.
- Liquefactive necrosis.
- Caseous necrosis.
- Coagulative necrosis.
- Fat necrosis.
- Patchy, transmural inflammation.
- Continuous inflammation limited to the colon, primarily affecting the mucosa and submucosa.
- Involvement of the entire GI tract.
- Skip lesions.
- Permanent destruction of alveolar walls.
- Fibrosis, smooth muscle hypertrophy, and increased mucus glands in the bronchi.
- Reversible airway constriction only.
- Decreased collagen deposition.
- A large wound with tissue loss that heals by granulation.
- A wound with minimal tissue loss and edges that are approximated.
- A wound that is left open and then closed later.
- The formation of a large scar.
- Fat necrosis.
- Liquefactive necrosis.
- Muscle tissue breakdown and release of myoglobin.
- Coagulative necrosis.
- A genetic defect present at birth.
- Another underlying disease or treatment.
- Exposure to a specific allergen.
- Excessive production of antibodies.
- Physical agent.
- Infectious agent.
- Nutritional imbalance.
- Genetic defect.
- Arterial spasm in the lungs.
- A clot dislodges from a peripheral vein and travels to the pulmonary circulation.
- Inhaled foreign body.
- Direct lung infection.
- Increasing gastric mucus production.
- Inhibiting prostaglandin synthesis, which reduces gastric mucosal protection.
- Stimulating gastric acid secretion.
- Enhancing gastric blood flow.
- Pallor, numbness, decreased temperature.
- Redness, heat, swelling, pain, loss of function.
- Jaundice, itching, weight loss.
- Cyanosis, dyspnea, confusion.
- IgE-mediated mast cell degranulation.
- Antibody-dependent cellular cytotoxicity.
- Formation of immune complexes that deposit in tissues, causing inflammation.
- Delayed T-cell mediated response.
- Impaired hemoglobin synthesis.
- Abnormal chloride transport across cell membranes.
- Autoimmune destruction of pancreatic cells.
- Defective muscle protein.
- Inflammation of the bladder only.
- Chronic inflammation of the kidney parenchyma and renal pelvis.
- Glomerular inflammation.
- Formation of kidney stones.
- Vasodilation to increase blood flow.
- Activation of the sympathetic nervous system and renin-angiotensin-aldosterone system.
- Decreased heart rate.
- Increased urine output.
- Arterial vasodilation.
- Hardening and narrowing of arteries due to plaque buildup.
- Venous inflammation.
- Increased arterial elasticity.
- Autoantibodies attacking the neuromuscular junction.
- Systemic inflammation mediated by immune complexes and T-cells, primarily affecting synovial joints.
- Destruction of pancreatic beta cells.
- Increased red blood cell destruction.
- Enhanced immune function.
- Decreased blood glucose levels.
- Impaired immune function and increased risk of infection.
- Improved sleep patterns.
- Normal scar formation.
- Excessive collagen formation, extending beyond the original wound boundaries.
- Incomplete wound closure.
- Decreased tensile strength.
