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24-year-old (female) with hyperglycemia

by Mohammad Hajighasemi-Ossareh, MD

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    00:02 A 24 year old accountant is brought to the emergency room by her coworkers after they found her unconscious at her cubicle when they returned from lunch.

    00:06 after they found her unconscious at her cubicle when they returned from lunch.

    00:11 One of them tells you that she has diabetes but does not know anything more about her condition.

    00:15 They are trying to contact family members for more information.

    00:19 Her vitals reveal a pulse of 110, respirations are 24, temperature is 36.7 degrees celsius and blood pressure is 90/60.

    00:29 She is breathing heavily and gives irrelevant responses to questions.

    00:33 Her skin and mucous membranes appear dry.

    00:36 Examination of the abdomen reveals mild tenderness.

    00:39 Tendon reflexes are slightly delayed.

    00:42 Laboratory findings include: Finger stick glusoces of 630 (mg/dl) ABG reveals pH of 7.1, pO2 of 90 (mmHg), pCO2 of 33 (mmHg) and bicarb of 8 g/L Lytes include a sodium of 135 (mEq/L), Potassium of 3.1 (mEq/L), Chloride of 136 mEq/L, BUN of 20 (mg/dL) and creatinine of 1.2 (mg/dL) UA shows Glucose - positive, Ketones - positive, Leucocytes - negative, Nitrite - negative, RBC - negative, and casts - negative She is immediately started on a bolus of IV 0.9% Sodium Chloride.

    01:17 Which is the next best step in management of this patient? Answer choice (A) - Infuse bicarb slowly Answer choice (B) - Switch fluids to 0.46% or half NS Sodium Chloride Answer choice (C) - Start IV insulin infusion Answer choice (D) - Replete potassium intravenously Or answer choice (E) - Start IV 5% dextrose Now take a moment to come to your own conclusion before we go through it together.

    01:51 Okay let's jump right into this question together.

    01:54 First thing to do is determine the question characteristics.

    01:57 Now this question here concerns both pathology and pharmacology.

    02:01 First we have to determine the diagnosis of what this patient has and then determine the most urgent action picking our pharmacological agent.

    02:08 Now this is a 2-step question - diagnose then pick the agent.

    02:12 And the stem is absolutely required because we need to read the clinical history to determine the diagnosis and then we'll use the history in conjunction with the laboratory findings to find the next best intervention.

    02:24 Now let's walk through this question.

    02:25 Step 1 - let's determine the most likely diagnosis.

    02:28 Now this patient appears to have what's called diabetic ketoacidosis which is due to uncontrolled hyperglycemia.

    02:36 Now let's refer to our image of diabetic ketoacidosis to better understand the condition.

    02:42 Now if you look at the top of the image, it kinda goes through it and we'll look down together.

    02:46 In the setting of insufficient or absent insulin, in the conditions such as in diabetes where patients have insufficient or absent insulin, there is going to be a insulin-deficient state.

    03:00 And three different senarios will occur.

    03:02 We'll be looking at muscles, fat cells and also the liver.

    03:05 So let's look at the muscles first.

    03:08 In the insufficient or absent insulin state, first the muscles will be asked to break down and release amino acids which will then go to the liver and then in that process, it will be converted into glucose.

    03:20 Also if you look at the insufficient or absent insulin state going to fat cells, they will also break down into both glycerol and fatty acids which both go to the liver.

    03:30 Now the glycerol gets converted into glucose but the fatty acids actually get converted over to ketones.

    03:37 And then in the setting of the insufficient or absent insulin, you actually have increased glucagon secretion from the pancreas which then also goes to both fat cells to stimulate the release of glycerol and fatty acids and then also goes to the liver itself.

    03:57 And then the insufficient or absent insulin also get stimulated to the liver itself.

    04:03 And then the liver, by using both substances from amino acids, and glycerol and fatty acids and even other substances, actually glycogen itself which is a great storage in the liver will break down into glucose and the fatty acid will then get converted into ketones.

    04:18 So here we have glycogenolysis, gluconeogenesis and also ketogenesis.

    04:23 Now what's going to happen is we're going to have increased glucose production that goes into the system which is a response to having insufficient insulin and we're going to have increased ketones in the blood as well, which is why we call it diabetic ketoacidosis because of the ketones that are released and the acidotic state that results.

    04:44 So this is what happens in diabetic ketoacidosis.

    04:48 So let's go back to our walkthrough.

    04:50 We said here, for step 1, the patient has dabetic ketoacidosis due to uncontrolled hyperglycemia from insufficient or absent insulin.

    04:57 Now in this condition, the potassium is low, which is typical for diabetic ketoacidosis and is due to potassium depletion due to the increased diuresis.

    05:08 Now the pH is also low in this case but it's not below 7, so this wouldn't represent a severe acidosis.

    05:17 Now that we know what the patient has, let's refer to step 2 to determine our intervention.

    05:22 Now hypokalemia which is the low potassium level can be life-threatening and in this case, the patient's potassium is 3.1 Now given that hypokalemia can be life threatening, it will be exacerbated by insulin treatment if we were to give insulin right away to this patient to wanna treat their hyperglycemia because giving insulin, as glucose enters the cells, it also will draw potassium into it making the hypokalemia even more severe which will even be more life-threatening.

    05:52 Thus, before starting IV insulin, it is important to replete potassium first via IV repletion of the potassium.

    06:01 This is an extremely high-yield point Let me say that one more time for the sake of making it clear.

    06:07 This is EXTREMELY high-yield important.

    06:10 You have to give potassium before starting your IV insulin for diabetic ketoacidosis.

    06:14 This is bread and butter internal medicine, you have to know this.

    06:17 You have to know it for USMLE.

    06:19 You also have to know it when you're on the wards because diabetic ketoacidosis is extremely common.

    06:24 You will be asked what to do. If you're a resident, you will be doing it.

    06:28 You don't want to make a mistake and harm a patient, so extremely important to learn this now.

    06:32 Replete the potassium before you start the IV insulin.

    06:36 It's okay.

    06:37 Now, what else here? Bicarb can also be given in a condition of diabetic ketoacidosis when patients have severe acidosis which is the pH of below 7, which in this case does not apply.

    06:50 Thus the correct answer in this case is answer choice (D) - replace potassium intravenously.

    06:55 Now let's go through some high-yield facts regarding diabetic ketoacidosis.

    06:59 Now diabetic ketoacidosis is a life-threatening complication of diabetes.

    07:04 Patients with diabetic ketoacidosis require rehydration and also IV insulin.

    07:09 But hypokalemia must be corrected with IV potassium before -remember that - before IV insulin is started as hypokalemia itself can be life-threatening and will be exacerbated by insulin therapy as glucose entering the cells draws potassium along with it.

    07:26 Now the use of IV bicarbonate in diabetic ketoacidosis should generally only be considered in severe acidosis which is a condition in which the pH is less than 7


    About the Lecture

    The lecture 24-year-old (female) with hyperglycemia by Mohammad Hajighasemi-Ossareh, MD is from the course Qbank Walkthrough USMLE Step 1 Tutorials.


    Author of lecture 24-year-old (female) with hyperglycemia

     Mohammad Hajighasemi-Ossareh, MD

    Mohammad Hajighasemi-Ossareh, MD


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