1. Hypokalaemia a) Describe three primary causes of hypokalemia. b) List the clinical signs and symptoms associated with severe hypokalemia. c) Outline the management plan for a patient with symptomatic hypokalemia. Answer: Conn’s disease , being on a loop diuretic medication , decreased dietary intake. Muscle weakness, arrhythmias, and decreased reflexes. Give them IV K+, find out the cause and reverse that. For example, if it is does to ADH could put the patient on a potassium sparing diuretic. 2. Hyperkalaemia a) Identify four potential causes of hyperkalemia. b) Explain the ECG changes associated with progressive hyperkalemia. c) Describe the emergency management steps for a patient presenting with severe hyperkalemia. Answer: metabolic acidosis such as in DKA, aldosterone insufficiency, potassium sparing diuretic and tumor lysis syndrome. Tall and peaked T waves, prolonged PR interval and a wife QRS complex. Give the patient IV fluids to dilute the K+ concentration, give the patient insulin, give the patient IV hydrocortisone if the cause is alderstone insufficiency, if the patient is in a potassium sparing diuretic, then cease that and consider changing it to a different medication such as loop diuretics. Give the patient calcium gluconate to help reverse or at least alleviate the effects on the heart symptoms. 3. Hyponatremia a) Define hyponatremia and classify it based on serum osmolality. b) List three common causes of hyponatremia in a hospitalized patient. c) Discuss the potential complications of rapid correction of hyponatremia. Answer: hyponatremia is when the sodium concentration in the blood stream is less than less than 135 mmol/L. adrenal insufficiency, SIADH, CHF osmotic demyelination syndrome. This is because overcorrecting Na+ or correcting Na+ too fast leads to hypernatremia since Na+ is osmotically active it will draw water and fluids out of cells -> this includes neurons such as the oligodendrocytes -> this will cause rapid fluid movement out of them -> will cause them to shrink -> oligodendrocyte death -> decreased myelination of the CNS. Other complications include seizures, muscle weakness, and altered muscle weakness due to the electrolyte imbalances. 4. Hypernatremia a) Explain two mechanisms that can lead to hypernatremia. b) Describe the clinical features of hypernatremia in elderly patients. c) Outline the management principles for correcting hypernatremia in a chronic setting. Answer: Conn’s syndrome. This happens because there is an increase in aldosterone -> increase Na+/K+ ATPases -> increased Na+ reabsorption and decrease in Na+ excretion -> increased concentration of Na+ in the bloodstream -> hypernatremia. Diabetes insipidus: either ADH deficiency or impaired renal response to ADH -> decrease water reabsorption -> decrease in Na+ dilution -> hypernatremia. Hypertension due to increase in vasoconstriction force seizures, delirium, muscle weakness due to electrolyte imbalances, Give IV fluids to dilute Na+ to determine how much fluid to give them find out FWD and the TWB. Find out the cause and manage that. For example, if due to diabetes insipidus -> give vasopressor. 5. Hypocalcemia a) Describe three causes of hypocalcemia. b) What are the key clinical signs of hypocalcemia? Include specific signs observed on physical examination. c) Outline the acute treatment for symptomatic hypocalcemia. Answer: hypoparathyroidism, CKD , Crohn’s disease arrythmias, chvoske’s sign and trousseau sign give the patient calcium, give the patient magnesium , give the patient vitamin D and recombined PTH 6. Hypercalcemia a) Name four common causes of hypercalcemia. b) Explain the pathophysiology behind hypercalcemia’s effect on renal function. c) Summarize the initial management approach for a patient presenting with severe hypercalcemia. Answer: primary or tertiary hyperparathyroidism , increased vitamin D intake, osteolytic bone cancer, sarcoidosis, paraneoplastic PTH such as in squamous cell lung cancer. High calcium levels -> more calcium goes to the kidney -> more free calcium -> increased binding to free phosphate or oxalate -> stone formation -> can lead to hydronephrosis or post-renal AKI or both. Dilution with IV fluids, calcimimetics , bisphosphates 7. Hypophosphatemia a) List three causes of hypophosphatemia in critically ill patients. b) Describe the physiological role of phosphate in cellular energy production. c) Outline the management strategy for moderate-to-severe hypophosphatemia. Answer: Hypoparathyroidism, low vitamin D intake and increased renal excretion. It helps with ATP production which we need for active transport, such as from the Na+/K+ ATPase. Give the patient recombinant PTH , vitamin D supplements and phosphate supplements. 8. Hyperphosphatemia a) Identify three causes of hyperphosphatemia. b) Discuss the complications associated with chronic hyperphosphatemia in patients with renal impairment. c) Explain the management approach, including dietary and pharmacologic measures, for hyperphosphatemia in renal disease. Answer: Primary Hyperparathyroidism, secondary hyperparathyroidism, osteolytic bone cancer, ectopic PTH secretion such as in squamous lung cancer, increased vitamin D intake. Nephrolithiasis, muscle cramps, arrythmias, seizures. Calcimemetics , give the patient bisphophates and IV fluids to dilute. Ditary measures would be to reduce phosphate intake such as almond and fish.