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- HDL cholesterol normal range is______in ______mg/dL (enter greater-lessthan as "<" or ">) (note: not 40,60,or 200 mg/dL, but is > in____)op of Form Normal Levels of Substances in the Arterial Blood: pH 7.40 + 0.05 pCO2 (partial pressure of carbon dioxide) 40 mm Hg pO2 (partial pressure of oxygen) 90 - 100 mm Hg Hemoglobin - O2 saturation 94 - 100 % [HCO3-] 24 meq / liter Vignette #1: A 21-year-old noncompliant female with a history of type I (insulin-dependent) diabetes mellitus was found in a coma. Her blood glucose was high, as well as her urine glucose, urine ketones, and serum ketones. Her serum bicarbonate was < 12 mEq/L. Her respiration was exaggerated, and her breath had an acetone odor. Her blood pressure was 90/60 and his pulse weak and rapid (120). 1. Define noncompliant. 2. Is this person experiencing ketoacidosis or insulin shock? Explain your answer. 3. Why is the serum bicarbonate low? 4. What is the acid-base status of this individual? 5. What are the causes of the dyspnea, hypotension, and tachycardia? 6. What type of treatment does this person need?…CC was taken to hospital breathing but unresponsive after two days of heavy alcohol consumption and limited food intake. According to CC's past medical history they had a history of chronic alcohol addiction and fatty liver disease. Analysis of CC's serum glucose returned a value of < 20 mg/dL, indicating severe hypoglycemia. The attending physician prescribed a bolus of D-glucose to help re-establish CC's blood glucose to within normal bounds. Analysis of the CC's serum electrolytes and PaCCh was suggestive of metabolic acidosis. Analysis of CC's blood suggested metabolic acidosis. In CC's case, what can cause metabolic acidosis?
- CC was taken to hospital breathing but unresponsive after two days of heavy alcohol consumption and limited food intake. According to CC's past medical history they had a history of chronic alcohol addiction and fatty liver disease. Analysis of CC's serum glucose returned a value of < 20 mg/dL, indicating severe hypoglycemia. The attending physician prescribed a bolus of D-glucose to help re-establish CC's blood glucose to within normal bounds. Analysis of the CC's serum electrolytes and PaCO2 was suggestive of metabolic acidosis. Q1: Which of the following metabolites may be used to produce blood glucose during prolonged fasting?Explain the physiological mechanisms involved in blood glucose concentration regulation trying to prevent hypoglycemia which is especially dangerous for brain function.A new drug was developed and found to be primarily eliminated by hepatic metabolism; i.e., the drug was not excreted in urine or secreted into bile. metakof the metabolic reaction is 2 mg/L and its Vmax is 125 mg/d. Using the Michaelis-Menten equation, calculate the rate of metabolism when the plasma drug concentration [C,] is as shown in the table below. [C,] mg/L Rate of Metabolism (mg/d) 0.025 0.050 0.10 0.20 0.5 1.0 2.0 4.0 10 20 40 60 Plot a graph with concentration on the X-axis and rate of metabolism on the Y-axis. Note how the reaction rate increases proportionately with plasma concentration at low concentrations (first-order kinetics), and then approaches saturation (Vmax) at high concentrations. nictored orally as a 159 mg tablet. During
- In a different instance of two infants suspected to have a defi- ciency of the PDH complex because of severe lactic acidosis, tissue biop- sies could not be taken to measure URINARY EXCRETION OF PYRUVIC AND a-KETOGLUTARIC ACIDS Pyruvic Acid (итol/ mg of creatinine) a-Ketoglutaric Acid (µmol/mg of creatinine) Age Special Diet or Drugs Patient G. M. 5 wk 2.26 3.57 enzyme activities. Instead it was no- ticed that there were high concentra- tions of organic acids in the urine. Typical results are tabulated in the ta- ble on the right. Identify the enzyme defect and explain why it presents this metabolic pattern. What other meta- bolic breakdown products likely were also detected especially following a high protein diet but are not listed? Name the defective enzyme. 7½ wk 2.10 3.39 11 wk 1.35 4.63 12 wk After 18-hr fast 1.87 0.44 High-protein, low-carbohy- drate diet 15 wk 1.62 5.38 Patient D. M. 1 day 13 days 0.87 0.44 Thiamine 0.45 3.44 24 days 0.33 2.47 4 wk 0.53 1.23 6 wk Thiamine 0.42…During strenous exercise, glucose is primarily converted to?A 35-year-old woman became severely depressed after the sudden death of her husband. Twomonths later, she was brought to the emergency room by her friend because of extremeweakness and lethargy. She appeared thin and pale. Upon history taking, the doctor found thatshe had not eaten for several weeks. Analysis of the plasma sample indicated elevated levels ofalanine, acetoacetate, β-hydroxybutyrate and blood urea nitrogen (BUN). However, her plasmaglucose concentration was low (55mg/dL). She was hospitalized, given intravenous feeding,antidepressant medications and subsequently shifted to a 1800kCal (7500kJ) diet. Her recoverywas uneventful.3.a) How could the patient maintain her plasma glucose levels within normal limits even though shewas not eating?b
- Insulin Lispro subcutaneously for a patient weight 80 kg for 1 month of treatment. Daily dose of insulin is 1 Unit/kg and 60% in short acting, given 4 times per day; ampoules in form of personal injectors (300 Units/3ml). (I would like to figure out the number of personal injector needed for 1 month.) My answer: Daily dose (DD) for a 80 kg patient = 80 x 1 Unit = 80 U 60% is short acting, so DD = 60% of 80 U = (0.6 × 80) U = 48 U Given 4 times per day, so for a single dose = 48 U/4 = 12 U For 1 month (30 days), 30 x 48U = 1440 U Rp. Insulin lispro in ampoules personal injectors 300 Units/3 ml No. ??? (my teacher write is 10 but I don't understand why) Sig. Inject subcutaneously 12 Unit (0.12 ml) before each meal, 4 times a day for 1 month.How many ml of u-500 insulin suspension will provide a dose of 150 units of insulinThe concentrations of lactate in blood plasma before, during, and after a 400 m sprint are shown in the graph.(a) What causes the rapid rise in lactate concentration?(b) What causes the decline in lactate concentration after completion of the sprint? Why does the decline occur more slowly than the increase?(c) Why is the concentration of lactate not zero during the resting state?