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Questions of presentation Note: Every question should be matched a ppt, which is going to be better if attached picture, concept map and painting on the blackboard etc. If the speaker just read the ppt, will not explain a question with your own words clearly, methodically and logically, you will get less marks on the part of personal performance. 1. Please briefly introduce the regulation of potassium homeostasis and the function of potassium. 2. Please explain the potassium distribution inside and outside cell. What are the hypokalemia and hyperkalemia? 3. Please explain how hyperkalemia effects on the excitability of skeletal muscle? Discuss the changes in resting membrane potential (Em) and the threshold potential (Et) in hyperkalemia. 4. Please describe the effects of hyperkalemia on myocardial physiological character (excitability, conductivity, automaticity, contractility), and the main ECG changes in hyperkalemia. 5. The friends of a 26-year-old man, who is scheduled to be married in a month, plan a bachelor’s party for him in Las Vegas. After a round of golf in 100°F weather, the group heads to the pool. They order several rounds of drinks over the next 4 hours and also order lunch poolside. Most of the group orders hamburgers and french fries, but the groom-to-be is watching his weight and opts for a club sandwich and a side of coleslaw. Later that night, they go for dinner and to the casinos, where they imbibe some more. Early next morning, the groom-to-be becomes ill. He thinks it is just a hangover, but presents to the emergency department 36 hours later with persistent vomiting and orthostatic hypotension. Question: What kinds of metabolic abnormalities (anyone you have studied) are most likely present in this patient? Why? 1 Hint: Severe vomit may lead to electrolyte disorder, body fluid disorder and acid and base disorder. 6. A 56-year-old woman with chronic renal disease was brought to the emergency department due to severe vomiting. She complained of vomiting and generalized weakness. On physical examination, she was lethargic, with poor skin turgor, a supine blood pressure of 110/90mmHg and a standing blood pressure 93/60 mmHg. Her body temperature was 37°C, pulse 120 beats/min. Laboratory results showed serum sodium was 110mmol/L; serum potassium dropped to 2.5mmol/L, and arterial pH was 7.6. Electrocardiogram demonstrated flatted T waves and prominent U wave. Question: Which type of potassium disorder is likely present in this patient? Why? Please describe the main ECG changes in this type of potassium disorder. 7. Same as the previous case, to be continued: After intravenous infusion of 0.9% NaCl solution and oral KCl replacement, electrocardiogram revealed peaked T waves. The patient was treated with insulin and glucose, followed by hemodialysis, and the electrocardiogram returned to normal. Question: why did peaked T waves present on the ECG after treatment? Why did treat this patient with infusion of insulin and glucose? Please briefly introduce hemodialysis. 8. Please explain the therapeutic principle for the hyperkalemia and its mechanism (why does the treatment work?) 9. What is the acute renal failure (ARF)? Please further explain the etiology and classification (pre, intra and post-renal). 10. Which alterations of metabolism and function may occur in acute renal failure? Which one is the most dangerous and need to be corrected immediately? 2 11. What is the chronic renal failure (CRF)? What’s the uremia? What’s the difference between them? 12. Please explain the pathogenesis of renovascular hypertension. 13. Please explain the pathogenesis of renal osteodystrophy combined with the disorder of Calcium, phosphate and bone metabolism in chronic renal failure. 14. A 54-year-old man with a history of type 2 diabetes and coronary artery disease is admitted to the coronary care unit with worsening angina and hypertension. His pain is controlled with intravenous nitroglycerin, and he is treated with aspirin, beta-blockers to lower his heart rate, and angiotensin-converting enzyme (ACE) inhibitors to lower his blood pressure. Cardiac enzymes are normal. He under- goes coronary angiography, which reveals no significant stenosis. By the next day, his urine output has diminished to 200 mL over 24 hours. Examination at that time reveals that he is afebrile, his heart rate is regular at 56 bpm, and his blood pressure is 109/65 mm Hg. His fundus reveals dot hemorrhages and hard exudates, his neck veins are flat, his chest is clear, and his heart rhythm is normal with an S4 gallop and no murmur or friction rub. His abdomen is soft without masses or bruits. He has no peripheral edema or rashes, with normal pulses in all extremities. Current laboratory studies include Na+140 mEq/L, K+5.3 mEq/L, Cl-104 mEq/L, and blood urea nitrogen (BUN) 69 mg/dL. His creatinine (Cr) level has risen to 2.9 mg/dL from 1.6 mg/dL on admission. Question: What is the patient’s new clinical problem? Why? What is the clinical meaning of blood urea nitrogen (BUN) and creatinine (Cr)? 3