Download 2. Questions of presentation

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?
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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?
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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)?
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