- Increases glucagon secretion.
- Mimics incretin hormones, stimulating glucose-dependent insulin release, suppressing glucagon, and slowing gastric emptying.
- Increases glucose absorption.
- Decreases insulin sensitivity.
Category: Pathophysiology-II
- Bowel obstruction.
- Inflammation and autodigestion of the pancreas by activated enzymes.
- Gastric acid reflux.
- Appendicitis.
- Risk of hypernatremia.
- Risk of accidental parathyroid gland removal, leading to hypoparathyroidism and life-threatening hypocalcemia.
- Risk of hyperkalemia.
- Risk of hypoglycemia.
- Increased platelet count.
- Impaired synthesis of clotting factors by the damaged liver.
- Increased fibrinolysis.
- Decreased red blood cell production.
- Oral medications for blood sugar.
- Initiation of renal replacement therapy (dialysis or kidney transplant) to sustain life and manage complications.
- Only dietary modifications.
- No urgent intervention needed.
- Increased potassium intake.
- Renal potassium wasting due to increased bicarbonate and volume depletion, and intracellular shift of potassium.
- Decreased aldosterone.
- Decreased renal excretion.
- Vasodilation.
- Thrombosis formation on the ruptured plaque, leading to partial or complete coronary artery occlusion.
- Spasm of coronary artery.
- Increased myocardial oxygen supply.
- To immediately start dialysis.
- To identify and urgently relieve the obstruction to urinary outflow (e.g., catheterization, stone removal).
- To administer loop diuretics.
- To prescribe antibiotics.
- Viral infection.
- DNA damage and mutations in lung cells induced by carcinogens in tobacco smoke.
- Autoimmune reaction.
- Bacterial infection.
- To stimulate glucagon release.
- To replace the absolute deficiency of endogenous insulin.
- To decrease insulin resistance.
- To delay glucose absorption.
- Rapid ventricular filling in a dilated ventricle.
- Atrial contraction against a stiff, non-compliant ventricle.
- Valvular regurgitation.
- Pericardial friction rub.
- Oral fluids.
- Administration of hyperosmolar agents (e.g., mannitol) or hypertonic saline to reduce cerebral edema.
- Oral antibiotics.
- Only observation.
- Increased cerebral blood flow.
- Cerebral vasoconstriction due to decreased PCO2? and decreased ionized calcium.
- Decreased oxygen levels.
- Increased heart rate.
- Peripheral neuropathy.
- Bacterial colonization and vegetation on heart valves, potentially leading to septic emboli and systemic infection.
- Autoimmune response.
- Valvular calcification.
- Direct kidney damage.
- Severe renal vasoconstriction in the setting of advanced liver disease, without primary kidney pathology.
- Kidney stones.
- Glomerular inflammation.
- Excess catecholamines.
- Deficiency of cortisol and aldosterone, leading to volume depletion and vascular collapse.
- Increased blood pressure.
- Excess insulin.
- Increased bone formation.
- Impaired calcium and phosphate homeostasis, leading to bone remodeling abnormalities.
- Decreased parathyroid hormone.
- Increased Vitamin D activation.
- To alleviate pain.
- To urgently achieve reperfusion of the ischemic myocardium to limit infarct size and preserve cardiac function.
- To prevent infection.
- To reduce fluid overload.
- Increases insulin secretion.
- Inhibits sodium-glucose co-transporter 2 in the renal tubules, leading to increased glucose excretion in the urine.
- Decreases hepatic glucose production.
- Increases insulin sensitivity.
