- Immediate surgery.
- Conservative management with NPO, IV fluids, and nasogastric tube until bowel function returns.
- Oral laxatives.
- Administration of opioids only.
No category found.
- Atrial contraction against a stiff ventricle.
- Rapid ventricular filling in a dilated and failing ventricle.
- Valvular stenosis.
- Pericardial friction rub.
- Acute inflammation of nerve endings.
- Damage to nerve fibers due to chronic hyperglycemia and microvascular complications.
- Demyelination due to autoimmune attack.
- Compression of spinal nerves.
- To reduce heart rate.
- To increase systemic vascular resistance and blood pressure to improve tissue perfusion.
- To decrease cardiac output.
- To increase urine output.
- To retain CO2?.
- To increase CO2? excretion to compensate for the metabolic acidosis.
- To increase oxygen intake.
- To decrease respiratory rate.
- Pre-renal AKI.
- Intrinsic (intra-renal) AKI.
- Post-renal AKI.
- Chronic kidney disease.
- Increased bone density.
- Reduced bone density and structural integrity, leading to increased fracture risk.
- Increased bone formation.
- Normal bone remodeling.
- Myocardial infarction.
- Pneumothorax.
- Aortic dissection, requiring urgent surgical consultation and blood pressure control.
- Pulmonary embolism.
- Impaired gastric emptying.
- Fibrosis and scarring of the esophageal wall.
- Acute inflammation.
- Muscle spasm.
- Vasodilation and decreased fluid retention.
- Vasoconstriction, sodium and water retention, and cardiac remodeling, leading to worsening heart failure.
- Improved cardiac contractility.
- Decreased afterload.
- Oral antacids.
- Administration of bicarbonate (if severe) and addressing the underlying cause of AKI.
- Hyperventilation.
- Loop diuretics.
- Acute inflammation of the retina.
- Microvascular damage and abnormal blood vessel growth in the retina due to chronic hyperglycemia.
- Optic nerve damage.
- Increased intraocular pressure.
- Normal immune function.
- Severe immunosuppression due to CD4+ T cell depletion.
- Hyperactive immune response.
- Autoimmune disease.
- Decreased intracranial pressure.
- Increased intracranial pressure (ICP), leading to brain herniation and neurological deterioration.
- Improved cerebral blood flow.
- Enhanced neurotransmission.
- Oral antibiotics.
- Surgical debridement of necrotic tissue and broad-spectrum antibiotics to prevent sepsis.
- Pain management only.
- Observation.
- Direct bacterial infection.
- Immune complex deposition in the glomeruli.
- Ischemic injury.
- Tubular damage.
- Neuropathic pain.
- Diabetic foot infection, often with osteomyelitis, requiring urgent antibiotic treatment and debridement.
- Ischemia only.
- Venous insufficiency.
- Obstruction of the urinary tract.
- Ischemic or nephrotoxic injury to renal tubular cells.
- Reduced renal perfusion.
- Glomerular inflammation.
- Increased potassium excretion.
- Shift of potassium from intracellular to extracellular space in exchange for hydrogen ions.
- Decreased potassium intake.
- Increased aldosterone.
