- Arterial spasm in the lungs.
- A clot dislodges from a peripheral vein and travels to the pulmonary circulation.
- Inhaled foreign body.
- Direct lung infection.
No category found.
- 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.
- White blood cells.
- Hemoglobin synthesis.
- Platelet production.
- Plasma volume.
- Bronchospasm.
- Massive pulmonary edema and severe hypoxemia due to capillary-alveolar membrane damage.
- Chronic airway inflammation.
- Alveolar wall destruction.
- Increased capillary hydrostatic pressure.
- Decreased plasma oncotic pressure.
- Increased lymphatic drainage.
- Increased arterial blood flow.
- Primary intention.
- Secondary intention.
- Tertiary intention.
- First intention.
- Alveolar wall destruction.
- Airway inflammation, mucus gland hyperplasia, and excessive mucus production.
- Reversible bronchospasm.
- Decreased peripheral airway resistance.
- The heart pumps blood efficiently.
- The heart's pumping ability is decreased.
- The heart valves are narrowed.
- The patient is experiencing fluid volume deficit.
- Necrosis.
- Apoptosis.
- Autophagy.
- Metaplasia.
- Red blood cells.
- Platelets.
- White blood cells.
- Plasma proteins.
