- Direct damage to kidney tubules.
- Obstruction of urine outflow.
- Decreased blood flow to the kidneys.
- Glomerular inflammation.
No category found.
- Klinefelter syndrome.
- Turner syndrome.
- Down syndrome.
- Cystic fibrosis.
- Gallstone obstruction only.
- Autodigestion of pancreatic tissue by its own enzymes.
- Increased insulin secretion.
- Liver inflammation.
- Atrophy.
- Hyperplasia.
- Metaplasia.
- Dysplasia.
- Initial sympathetic nervous system activation.
- Mobilization of resources and adaptation.
- Depletion of adaptation energy and potential for organ damage.
- Increased resistance to disease.
- Continuous inflammation limited to the colon.
- Patchy, transmural inflammation that can affect any part of the GI tract from mouth to anus.
- Ulceration limited to the mucosal layer of the rectum.
- Stricture formation only in the esophagus.
- Hypertension, obesity, and hyperlipidemia.
- Venous stasis, endothelial injury, and hypercoagulability.
- Hypovolemia, infection, and low blood pressure.
- Anemia, fever, and leukopenia.
- Absolute insulin deficiency due to autoimmune destruction.
- Insulin resistance and impaired insulin secretion.
- Excessive glucagon production.
- Pancreatic enzyme deficiency.
- Undergo apoptosis.
- Shrink in size.
- Spread from the primary site to distant organs.
- Become well-differentiated.
- Antibodies.
- Endotoxins.
- Pyrogens (e.g., IL-1, TNF-alpha).
- Histamine.
- Decreased capillary hydrostatic pressure.
- Increased plasma oncotic pressure.
- Increased capillary hydrostatic pressure due to fluid overload and decreased cardiac output.
- Increased lymphatic drainage.
- Allostasis.
- Homeostasis.
- Pathogenesis.
- Adaptation.
- Hypoxia.
- Free radicals.
- Chemical injury.
- Physical agents.
- Excessive use of loop diuretics.
- Diabetic ketoacidosis (DKA) with potassium shifting out of cells.
- Prolonged diarrhea.
- Cushing's syndrome.
- Autoantibodies that attack the body's own tissues.
- Increased complement proteins.
- Decreased inflammatory mediators.
- Excessive B-cell suppression.
- Bronchial smooth muscle hypertrophy.
- Alveolar wall destruction and loss of elastic recoil.
- Reversible airway inflammation.
- Increased mucus gland hyperplasia.
- Excessive clot formation leading to widespread microvascular thrombosis and consumption of clotting factors, followed by bleeding.
- Only excessive bleeding with no clot formation.
- Increased production of platelets.
- Decreased fibrinolysis.
- Autosomal dominant.
- Autosomal recessive.
- X-linked dominant.
- X-linked recessive.
- Increased intravascular protein synthesis.
- Decreased capillary permeability.
- Increased capillary hydrostatic pressure and increased capillary permeability.
- Decreased lymphatic drainage.
