- Hypoglycemia.
- Cardiac arrhythmias and potential cardiac arrest.
- Hypotension.
- Metabolic alkalosis.
Author: ETEA MCQS.COM
No category found.
- To increase heart rate.
- To block the effects of sympathetic nervous system activation, reducing myocardial oxygen demand and improving cardiac remodeling.
- To increase preload.
- To dilate peripheral blood vessels.
- Increases insulin secretion from the pancreas.
- Decreases hepatic glucose production and increases insulin sensitivity.
- Delays glucose absorption from the gut.
- Increases glucose excretion in the urine.
- Appendicitis.
- Gastroenteritis.
- Perforation of a peptic ulcer, leading to peritonitis.
- Irritable bowel syndrome exacerbation.
- Excess cortisol production.
- Autoimmune destruction of the adrenal cortex, leading to deficiency of cortisol and aldosterone.
- Excess aldosterone production.
- Impaired glucose metabolism.
- Bronchoconstriction.
- Alveolar consolidation with pus and exudate, impairing gas exchange.
- Pulmonary embolism.
- Reduced cardiac output.
- Oral antihistamine.
- Immediate administration of epinephrine.
- Topical steroid cream.
- Observation.
- Degeneration of articular cartilage.
- Autoimmune inflammation of the synovial membrane.
- Deposition of uric acid crystals.
- Bacterial infection of the joint.
- Decreased oncotic pressure.
- Increased hydrostatic pressure in the pulmonary capillaries due to left ventricular dysfunction.
- Increased lymphatic drainage.
- Decreased capillary permeability.
- Peptic ulcer.
- Pancreatitis.
- Gallstone obstruction of the cystic duct (biliary colic).
- Appendicitis.
- Administering high-flow oxygen.
- Initiating non-invasive positive pressure ventilation (NIPPV) or mechanical ventilation.
- Encouraging deep breathing exercises.
- Prescribing oral antibiotics.
- Hypovolemia.
- Bilateral ureteral obstruction.
- Acute tubular necrosis (ATN) due to prolonged renal ischemia.
- Glomerulonephritis.
- Abnormal chloride channel function, leading to thick, viscous secretions.
- Impaired ciliary movement.
- Alveolar destruction.
- Bronchial hypersensitivity.
- Direct inflammation of the renal parenchyma.
- Distension of the renal capsule and ureteral spasm.
- Ischemia of the kidney.
- Nerve compression in the spinal cord.
- Glomerular hyperfiltration.
- Direct tubular damage from myoglobin casts.
- Increased erythropoietin production.
- Renal artery stenosis.
- Increases reabsorption of sodium and water.
- Blocks aldosterone receptors.
- Inhibits sodium and chloride reabsorption in the loop of Henle, leading to increased diuresis.
- Decreases heart rate.
- Complement activation.
- Autoantibody production.
- Massive release of histamine and other inflammatory mediators from mast cells and basophils.
- T-cell mediated cytotoxicity.
- Acute inflammation of nerve endings.
- Demyelination due to autoimmune attack.
- Microvascular damage and metabolic alterations affecting nerve fibers.
- Compression of spinal nerves.
- Oral analgesics.
- Needle decompression for tension pneumothorax.
- Inhaled bronchodilator.
- IV antibiotics.
