Hi everyone, welcome back! Or if you're new here, welcome! My name is Nurse Jenny and I'm from Nurse Life Academy and I will be reviewing endocrine questions and concepts that you must know for the CCRN exam in this video.
I will time mark it, so just feel free to scroll at your own pace, but I do give extra information and explanations after every question to really reinforce the content. I would greatly appreciate if you like and subscribe to my video if you found it helpful. but also so that you can be notified of other videos dropping.
Let's get started with this endocrine content. Question number one. Which of the following medications may mask initial signs of hypoglycemia, such as shakiness, increased heart rate, and irritability? Is it A, glipizide, B, metoprolol, C, insulin glargine, or D, Hydrochlorothiazide.
And the answer here is B, metoprolol. So when someone becomes hypoglycemic, usually the sympathetic nervous system will kick in, and it'll trigger you to sweat, have palpitations, get anxious, maybe shaky, and then it increases your heart rate. And all of these symptoms are initial signs we would see if someone gets hypoglycemic. However, if you're on beta blockers such as metoprolol, those beta blockers are blocking that sympathetic response that we would normally see. And if these symptoms are blocked, unfortunately, sometimes the first symptoms that you'll see when someone's hypoglycemic may be those later ones, such as lethargy or even a coma.
So acute hypoglycemia is usually when a diabetic's blood sugar falls below 70, but it can also occur with big shifts in glucose. Some symptoms of hypoglycemia that you'll see, early on you'll have palpitations, tachycardia, diaphoresis, irritability, blurred vision, slurred speech, fatigue, weakness, and so forth. Later on, you'll have confusion, lethargy, seizure, and coma.
But again, remember from our question, if you have a diabetic who is also taking beta blockers, that initial sympathetic response may be masked due to the beta blockage. So they might be hypoglycemic, but you might not know until they present with some of those later symptoms such as confusion, lethargy, seizures, or coma. And in talking about causes, it seems quite simple, but a lot of the time the dose of insulin is more than what is necessary for the body requirements. Sometimes increased physical activity or strenuous activity can be a precursor to hypoglycemia for diabetics since you use up that glucose during exercise.
Also, things like stress, interrupted nutrition, or adrenal insufficiency may also be causes. The treatments are listed here. Essentially, you want to give them some source of glucose.
If the patient is conscious, giving them a glucose gel, maybe some juice, or some complex carbohydrates would all be pretty appropriate. And if they have IV access but they're unconscious, You would usually give a half amp or even a full amp of dextrose 50% depending on their blood sugar, and you may want to consider starting them on either a 5% or a 10% dextrose drip for refractory hypoglycemia if there are no other contraindications. Lastly, if they're unconscious without IV access, glucagon 0.5 to 1 mg IM is going to be your treatment. Question number two. Your nurse coworker cannot remember the normal values of serum osmolality and urine-specific gravity.
You tell her, I know a normal serum osmolality range is blank, milliosmoles per kilogram, and a normal urine-specific gravity is blank. Is it A, 260 to 275 and 1.010? B, 275 to 295 and 1.030?
260 to 296 and 1.030? Or is it D, 275 to 295 and 1.010? Thank you.
Thank you The answer here is D, 275 to 295 for the serum osmolality range, and a normal urine-specific gravity is 1.010. So let's talk a little bit about some endocrine basics here. Your serum osmolality is the measure of the number of particles or solutes in one's blood.
And the normal serum Osmo is about 275 to 295 milliosmoles per kilogram. You do need to memorize this normal range for Osmo. So 275 to 295. Now I did put the formula to determine the osmolality concentration, but don't worry, you do not need to memorize this.
I only put it here so that you can see that a change in either sodium, BUN, or glucose is going to alter your osmolality. And in the case of SIADH and DI, we will certainly have a change in sodium. So in both of them, we're going to have changes in our osmolalities. Urine specific gravity, or USG, is the measure of the concentration of the solutes in the urine. So it's very similar to serum osmo, but it just measures the solutes that are in the urine instead of the blood.
And a normal urine specific gravity is 1.010, or I remember easily as 1010. And when urine is dilute, or it has a low number of solutes, your urine specific gravity is going to be less than 1.010. So in this case, a low urine specific gravity would be 1.005. And on the other hand, If urine is very concentrated, it is going to have a high number of solutes.
So you will have a high urine specific gravity. So an example would be 1.030. Now, I don't want to confuse anyone, but sometimes I think about urine specific gravity in weight. So if your urine is very dilute, it is going to have a low number of solutes.
And in my head, I think low number of solutes. it's going to be light. So it's going to be a lower number than that normal of 1010 or 1.010.
But if urine is very concentrated, it's going to have a large amount of solutes and it's going to be heavier. So that number is going to be greater than that normal of 1010 or 1.010. Knowing what serum osmo and urine specific gravity are and their normal ranges is really going to help you out here. Let's switch gears here and quickly talk about ADH or antidiuretic hormone. So ADH is a hormone that is formed in the hypothalamus and it is stored in the posterior pituitary and its main function is to maintain fluid balance.
And if you guys remember, ADH is a part of the RAS pathway, the renin-angiotensin-aldosterone system. And And ADH can be stimulated and released by many things, but mainly it will respond to hypotension, hypovolemia, hypernatremia, or dehydration. So when you have a low serum osmo.
And when any of these problems are present, so if you're hypotensive, hypovolemic, dehydrated, whatever it may be, your body senses that and it releases ADH in order to compensate and hold onto that water. Or technically speaking, it reabsorbs water in the kidneys, which then stays in the vascular system because it doesn't want to give it up. So if ADH causes the body to reabsorb more water, then it's not going to release that water in the urine. So we can also say that it concentrates urine.
I know it's a little bit tricky to visualize this pathophysiology, but at the very least, if you break down the word anti-diuretic. You will not diurese and urinate out a lot of urine. Instead, you will concentrate urine and your body will hold on to that extra water.
So hopefully this makes a little bit of sense. It's always helpful, at least for me, to know the pathophysiology behind some of these conditions in order to be able to better understand what's going on. Question number three. Which of the following are signs of syndrome of inappropriate antidiuretic hormone, or SIADH? Secretion.
A, decreased urine output, increased serum osmolality, and hypernatremia. B, increased urine output, increased serum osmolality, and hypernatremia. C, increased urine output, decreased serum osmolality, and hyponatremia. Or D, decreased urine output, decreased serum osmolality, and hyponatremia. The answer is D, decreased urine output, decreased serum osmolality, and hyponatremia.
So in SIADH, you are swimming in ADH. And all of this ADH will lead to water retention in the body. So if you're going to be retaining a ton of water in your body, that intravascular space is going to be quite dilute, right?
You will have a decreased serum osmolality because the concentration of solutes in your blood is going to be lower. That goes hand in hand with the concentration of sodium. It's going to be low because of all that excess water.
Now, if your body retains all the water, it's not going to pee much out, so you're going to have a low urine output. Let's talk about SIADH, or Syndrome of Inappropriate Antidiuretic Hormone. And this is a condition where your body makes too much ADH.
I like to remember this by thinking swimming in ADH, because it has the letters SIADH in there, and it's a super easy way to remember it. So we know that secretion of ADH leads to increased water absorption in the body. So it holds onto that water and it doesn't want to pee it out because the body needs it for something.
If you're hypotensive, hypovolemic, or dehydrated, your body senses that and it wants to keep that water. So if you think about excess water in the body, the extra water it's holding onto is going to dilute the solutes that are in your vessels. So you'll have a...
decreased serum sodium, and a decreased serum osmolality. And again, since your body is holding onto that water and it's not peeing it out, you are going to have a low urine output, but a high urine specific gravity. Because remember, you're going to only have a little bit of urine, but whatever urine you have, it's going to be very concentrated.
And that concentration of solutes is going to be high. Thus, a high urine-specific gravity. So now that we know what happens when we have SIADH or we are swimming in ADH, how does this happen? Well, the three main causes include oat cell carcinoma, viral pneumonia, or head problems like a stroke or an intracranial hemorrhage or some kind of head trauma, TBI, anything like that.
And what are some of the complications? So... one of the biggest ones is the severe dilutional hyponatremia that we see with SAADH.
It is a classic sign of SAADH. Your sodium will be low, even into the one teens or the one twenties, and with such low sodiums, patients are at extremely high risk of seizures, so you must be very careful and you have to initiate seizure and fall precautions for these patients. In order to not decrease their sodium even further, we'll also restrict their water intake. So if they drink all that water, that water is going to dilute their sodium even more, so we really need to monitor them closely with a free water restriction.
We're also absolutely going to correct their sodium in this case, but we don't want to correct it more than 6 to 8 milliequivalents per liter a day. And the reason for this is because there is a rare but a potential risk of something called osmotic demyelination syndrome, and this results in irreversible neurological damage. We generally use hypertonic saline such as 3% and do serial Q4 hour labs to make sure that the sodium isn't going up too fast, but remember no more than six to eight millquivs per liter a day. Question number four.
Which of the following laboratory findings would you expect in a patient with hyperthyroidism? A. Increased T3, increased T4 and decreased TSH, B, decrease T3, Thank decrease T4, and increased TSH, C, decrease T3, increase T4, and increase TSH, or D, increase T3, decrease T4, and decreased TSH.
you. The correct answer is A, increased T3, increased T4, and a decreased TSH. And for the purpose of the CCRN, your T3 and T4 will always either be up or down. You're not going to have one that's increased or normal or decreased or whatever.
However, what you will have is an inverse relationship between the T3, T4, and your TSH. In its simplest form, the thyroid has a large part in regulating the body's metabolism and energy. And the labs you're going to see to assess thyroid function include T3, T4, and TSH. TSH is going to be your most reliable lab to measure thyroid function.
To simplify this very succinctly, your hypothalamus senses when your body has low levels of thyroid hormones. So it triggers the release of thyroid. thyroid stimulating hormone, or TSH, from your pituitary gland. And the thyroid stimulating hormone, just as its name suggests, it stimulates the thyroid gland to release the thyroid hormones T3 and T4. And just as a little side note, T4 is an inactive hormone, but it's converted into T3, and that's really all there is to it.
You must know that T3, T4, and TSH, like I mentioned in the last slide, are inversely related. And what I mean by this is that in this feedback loop that your thyroid has, if your T3 and T4 levels are low, TSH is going to be stimulated and it will increase in order to make more of that T3, T4. And then on the other hand, when your T3 and T4 are too high, TSH is not going to be stimulated because it doesn't need to make any more hormones, so that level is going to be low. Question number five. A patient with a history of thyroid disease and a recent infection was brought to the ER by her sister.
The patient had a decreased level of consciousness, delayed deep tendon reflexes, bradycardia, and hypothermia. Based on this situation, the nurse should anticipate a need for A, propylthiouracil or PTU, B, iodine, C, IV levothyroxine or synthroid, or D, bumetanide or Bumex. The answer is C, IV levothyroxine or synthroid. So based on how this patient is presenting, what condition do we think that this patient has? She has symptoms of a slow metabolism.
So I'm thinking that this is a hypothyroid picture, even one of severe hypothyroidism or myxedema coma based on the severity of her symptoms. And if a patient is hypothyroid, hypothyroid and they're not able to produce their own thyroid hormone effectively, we need to supplement them with some synthetic T4 or IV levothyroxine. Hypothyroidism is the inadequate output of the thyroid gland, so it does not produce the appropriate amounts of thyroid hormones, and this results in a slow metabolism.
And the most severe form of hypothyroidism is hypothyroidism, where there is a severe deficiency of thyroid hormones, is known as myxedema coma, which may be life-threatening. Some causes include Hashimoto's thyroiditis, which is an autoimmune inflammation of the thyroid gland, perhaps a thyroidectomy where they remove the thyroid gland and you can't produce thyroid hormones. Maybe we treated their hyperthyroidism a little too well that we pushed them into hypothyroidism. or a pituitary tumor may be the cause, or even medications such as amiodarone or lithium.
And the symptoms here will be associated with a slow metabolism because they are just not producing enough thyroid hormones. Thank So I'm sure we've all heard this first one before. Oh, you know, I've gained some weight now that I'm older because my metabolism slowed down.
Yeah, maybe. But if it's weight gain that seems a little out of control based on your energy intake and expenditure, you. it could be hypothyroidism instead of just the age-old metabolism slowing down. Some other symptoms can include fatigue, fluid retention, or edema. And then in the severe case of hypothyroidism or myxedema coma, the slow metabolism symptoms will be severe.
So you will see things like altered level of consciousness, disorientation, hypothermia, bradycardia, slow shallow respirations. Just think everything is slow. It is slow and it's cold. And the lab profile that we will see for a patient with hypothyroidism includes low levels of T3 and T4 because remember, they are just not producing those thyroid hormones. However, the TSH is going to point which direction?
It's going to be inverse. Why? Because the TSH is revving up and it's working overtime in order to try to stimulate the thyroid.
thyroid so that it can increase those levels of T3 and T4. The treatment here is going to be levothyroxine, which we've talked about. It is a synthetic form of T4, which we know will then be converted to T3 to increase the body's metabolism and stay regulated. Question number six. A patient with type 1 diabetes is admitted with a hyperglycemic emergency.
Her blood glucose was 540 and her potassium was 6.2. Your immediate priority is going to be A. Beginning an insulin infusion B.
Restarting her home sub-Q insulin C. Lowering her potassium level or D. Consulting a dietician.
The answer is A, beginning an insulin infusion. So here we have a patient presenting with what looks like a DKA picture. We have a type 1 diabetic who is hyperglycemic.
And although it's quite tempting to want to decrease her high potassium, the correct answer here is going to be A, beginning an insulin infusion. And the reason for this is in a state of metabolic acidosis, hydrogen ions move into the intracellular space. And if you have a high potassium, in exchange, potassium leaves the intracellular space. So the movement of potassium into the extracellular space results in this hyperkalemia, yet the total body potassium hasn't increased.
So that serum potassium draw is actually a false elevation. And since insulin drives potassium into cells, as soon as you begin an insulin infusion, that potassium is going right back into the cell. Diabetic ketoacidosis or DKA.
It is common in type 1 diabetics who do not produce any insulin from their beta cells. And usually when type 1 diabetics go into DKA, it's a result of some kind of stressor on the body such as an illness, infection, trauma, surgery, pregnancy, etc. But also sometimes it can simply be because patients are non-compliant with their insulin administration and they need it.
So how are these patients going to present? Let's start with the obvious one of hyperglycemia. Their blood sugars will be greater than 250, but generally around the 300 to 800 range.
And just as the name diabetic ketoacidosis states, they are going to have a metabolic acidosis. They are going to have elevated serum and urine ketones. When your cells don't get the glucose they need for energy, your body begins to burn fat for energy.
And that's where you get these ketones from. And in DKA, there's going to be an anion gap. The anion gap is an equation which really just tells you if your electrolytes are out of balance, which they will be because in DKA patients, they are in a state of acid dopamine.
Also, because of the high serum glucose levels, these patients will present with polyuria in the early stages, also polydipsia and polyphagia, so excess urination, excess thirst, and excess hunger. These patients will also have Kussmaul's breathing and maybe an acetone or fruity odor to their breath, both from the increased ketones in the body. Lastly, these patients will have hyperkalemia.
like we just talked about, in the acidosis state of DKA. So again, acidosis causes potassium to rise due to this transcellular shifting, where the potassium moves into the extracellular space and it falsely elevates that serum potassium. You do have to know that potassium and pH have an inverse relationship.
So every 0.1 decrease in the pH results in a 0.6 increase in serum potassium. Again, it's not the actual true serum reading because of this acidosis. And remember that insulin drives glucose, water, and potassium into cells. So as soon as you start that insulin infusion, that potassium is going right back into the cell. The treatment for DKA is going to include starting this insulin drip because they don't have any endogenous insulin of their own.
And each facility has a different DKA protocol or algorithm that they follow in order to titrate these drips. But we really don't want to decrease the blood sugar by more than 50 to 100 milligrams per deciliter an hour. That's pretty standard. And we'll keep the insulin drip on until their glucose is normal and they're acidosis has resolved, at which point we'll usually overlap it with a transition to long-acting and short-acting insulin depending on the physician. Since type 1 diabetics don't produce any insulin at all, you want to make sure that they have some insulin at all times in their body.
You don't want to just abruptly discontinue a drip without giving any other form of insulin. It is important to know that patients can die from hypovolemia in DKA. So you have to give them fluid because they lose so much of it. We generally start with isotonic fluids such as 0.9 normal saline and then switch it over to 0.45 normal saline once the patient is stable.
And we do that in order to rehydrate those cells with that hypotonic solution. And then when your blood sugar gets to 250 or less, that's when we would add some dextrose to our fluids in order to prevent hypoglycemia. Question number seven.
You are taking care of a patient who is admitted for sepsis and has a history of adrenal insufficiency. Her condition is worsening and you suspect Addisonian crisis. What treatment would you anticipate for this patient?
Is it A, fluids and hydrocortisone IV, B, propylthiouracil, PTU, and beta blockers, C, fluids and regular insulin, Or D, desmopressin, DDAVP, and dextrose? The answer is... A, fluids and hydrocortisone IV. Patients in Addisonian or adrenal insufficiency crisis are going to need fluids and hydrocortisone.
These patients with adrenal insufficiency do not produce enough cortisol or aldosterone, which means that they need some kind of glucocorticoid as well as fluids. So we will talk about the acute stage of adrenal insufficiency or an Addisonian crisis, which is the most severe form of adrenal insufficiency. Addison's disease is an autoimmune disorder in which the adrenal glands do not produce enough cortisol and aldosterone. Just a reminder, cortisol is our body's stress hormone and it also produces glucose. And aldosterone, as we know from the RAS pathway, is involved in sodium and water absorption, Thank you.
and it maintains blood pressure. Some causes of an Addisonian crisis include some kind of stress response to the body, such as sepsis, trauma, head injury, or even an abrupt withdrawal of steroids. So if we have a deficit in these hormones of cortisol and aldosterone, we are going to see symptoms like altered mental status, Thank you. weakness, severe hypotension, nausea, vomiting, hypoglycemia, fever, and maybe abdominal pain since the adrenal glands lie on top of the kidneys.
And patients with Addisonian crisis are going to have low levels of cortisol, low blood glucose levels, and high ACTH levels. We just talked about the treatment in our question, but the treatment will be fluids and glucocorticoid replacement. If a patient is known to have adrenal insufficiency, we will treat them with hydrocortisone IV. And if a patient has no known history of adrenal insufficiency, we will treat them with another steroid, but it will be dexamethasone. And the reason behind that is because dexamethasone does not interfere with some of the diagnostic lab testing that we would do for Addison's disease to see if they had it.
Question number eight. Your patient is suspected to be in diabetes insipidus, or DI. Which of the following laboratory findings would be consistent with a diagnosis of DI? Is it A. Increased serum osmo, increased serum sodium, and decreased urine osmo.
B, increased serum osmo, decreased serum sodium, and increased urine osmo. C, decreased serum osmo, increased serum sodium, and increased urine osmo. Or D, decreased serum osmo, decreased serum sodium, and increased urine osmo.
The answer here is A. Increased serum osmo, increased serum sodium, and a decreased urine osmo. So in DI, you are not going to have a lot of ADH or antidiuretic hormone.
And this leads to water loss in the form of urination. So you will be peeing liters and liters of fluid, which will decrease your urine osmolality. And since you become intravascularly dry, your serum osmolality and serum sodium are going to increase. So what happens in DI or diabetes insipidus? Well, in SIADH, remember, they are swimming in ADH.
But in DI, it's the opposite. They do not have enough ADH. And we already know that ADH acts to conserve water in the body and to concentrate urine. But if we don't have any of it, well, that's just not going to happen.
And so what's the result? They're going to lose all that water. You are going to pee your life away.
These patients can sometimes urinate in astounding 6 to 24 liters of urine a day. And since you're peeing so much, that urine is going to be so dilute. That means you're going to have a low urine specific gravity because there will be a low number of solutes. And at the same time, since you're peeing out all of that water, there really isn't going to be much water left in your vessels. And as a result, your serum sodium concentration and your serum osmolality are going to increase.
Most causes of DI are either neurogenic or nephrogenic in nature. Neurogenic causes include traumatic brain injuries, tumors, anoxic brain injuries, And nephrogenic causes are generally due to decreased renal responsiveness to ADH. So just thinking of what DI does and its tremendous water loss in the urine, one important complication is going to be hypovolemia or hypovolemic shock.
They are at serious risk for being intravascularly depleted due to how much fluid they're losing. So what's our treatment here? Well, they don't have ADH, right?
Luckily for these guys, we have a medication called DDAVP or desmopressin. And desmopressin is a synthetic form of ADH. We also want to replace the fluid that they lost intravascularly, but we want to replete it slow.
We generally want to correct the fluid deficit over two to three days to minimize the risk of cerebral edema. Question number nine. Which laboratory determination is the preferred indicator in distinguishing between DKA and HHS?
A. Serum glucose, B. Serum sodium, C. Serum potassium, or D.
Serum osmolality? The answer is D, serum osmolality. So serum osmolality is generally normal or slightly elevated in DKA, but it is severely elevated in HHS. And although glucose is usually higher in HHS, it is not the preferred value in distinguishing the two.
Let's talk about hyperosmolar hyperglycemia syndrome, or HHS. So this is common in type 2 diabetics, where the beta cells of the pancreas do produce insulin, but there is some insulin resistance which results in an insulin deficiency. The causes are usually similar to those in DKA, such as the stressor on the body or noncompliance with medications.
These patients are profoundly hypovolemic and they can lose upwards of 6 to 9 liters of fluid per day. They will have a very elevated serum osmolality, again because they're dehydrated and they are dry. They will not produce ketones because they have enough endogenous insulin to prevent ketosis.
And they also won't be acidotic. They'll present with altered mental status, possibly polyuria, but they will have a high urine-specific gravity because their urine will have a lot of glucose in it. And because of these patients'significant fluid loss, the most important intervention is going to be fluid resuscitation because patients can die from this hypovolemia.
We start with isotonic fluids such as 0.9 normal saline and can switch over to 0.45 normal saline for cellular hydration, usually once their serum osmo is within a normal range. Your next priority is going to be an insulin infusion to get that blood sugar down, and again, same with DKA, we would add some dextrose to the fluids once the blood sugars are less than 250. Question number 10. Which of the following would be expected findings in a patient with hyperthyroidism? A. Tachycardia, diaphoresis, and weight gain. B.
Palpitations, tachycardia, and heat intolerance. C. Insomnia, anxiety, and bradycardia. Or D. Cold intolerance, bradycardia, and weight loss. The answer is B, palpitations, tachycardia, and heat intolerance.
So a patient with hyperthyroidism, you're going to see symptoms of a fast metabolism. Hyperthyroidism. It is a condition where there is too much thyroid hormone production.
So we're going to think fast metabolism here. And the most severe form of hyperthyroidism, where there is a severe overproduction of thyroid hormones, is known as thyroid crisis or thyroid storm, which may be life-threatening. The main causes of hyperthyroidism include Graves disease.
which is an autoimmune disorder that causes the body to attack the thyroid gland. Also, thyroid adenomas, nodular goiters, or infection can all be causes as well. Symptoms of hyperthyroidism include weight loss, tachycardia and palpitations, anxiety, agitation, diaphoresis, and heat intolerance. Again, you're thinking fast metabolism. And in thyroid storm, the severe presentation of these patients will include altered mental status, confusion, tremoring, severe tachycardia, tachycardia, and tachycardia.
tachypnea, and fever. Your labs are going to show a high T3 and T4 with an inversely related TSH because we do not need the TSH to be stimulated making any more thyroid hormone than we already have. Our treatment is going to include trying to decrease the amount of T3 and T4 the body makes and has. We're going to block T4 synthesis and We can do that with a medication called propylthiouracil, otherwise known as PTU, or methamazole.
We're going to block T4 to T3 conversion with PTU. We can also give a beta blocker called propranolol, which not only has beta blocking effects, but it also blocks conversion of T4 to T3. For hypothyroidism that can't be medically managed, a patient could get a thyroidectomy to remove the thyroid that is... overproducing these thyroid hormones as well. Question number 11. A 74-year-old patient who recently had viral pneumonia was admitted to the hospital for seizures.
Her BMP came back with a sodium level of 118 milliequivs per liter, a potassium level of 4.0, a BUN of 16, and a creatinine of 1.0. Her urine output has been 15 milliliters an hour over the last four hours and her urine specific gravity is 1.030. Her serum osmolality is 260 milliosm per kilogram. Which of the following would you expect ordered for this patient? A.
Administer antivirals. B. Administer D5 water at 100 milliliters an hour.
C. Free water restriction. or D, administered desmopressin, otherwise known as DDAVP.
So what endocrine condition are we talking about here? Is this SIADH or DI? Let's look at our labs here. So we have severe hyponatremia. We have low urine output, a high urine specific gravity.
We have this low serum osmo. We are looking at SIADH. And we are going to impose a free water restriction because we do not want to lower that sodium any lower than it is.
Okie dokes. So now that we have covered both SIADH and DI, if anyone is down for a little quiz to see how well you know the difference between the two, let's do it. If not, go ahead and skip ahead.
So let's go through the SIADH column first here. Our ADH level, is it going to be increased or decreased? Remember, in SIADH, we are swimming.
in ADH, so it is increased. What is our serum osmolality going to be? Okay, so if we're swimming in ADH, that means that we are holding on to all of this water and we are not letting it go. So if our blood is very dilute with that extra water, we are going to have a low concentration of solutes in the blood, right?
So that level is going to be decreased. Alright, moving on to our serum sodium, is it going to be increased or decreased? It's going to be decreased. Again, remember that intravascular blood is going to be super diluted with all that water it's holding on to. So our sodium is going to be decreased.
How about our urine specific gravity? What do we think? Well, we're not going to be peeing out a lot of water because that ADH is making us conserve it in our body. So we're going to have low urine output and it is going to be concentrated. And concentrated urine means that it's going to have a large concentration of solutes, making that urine specific gravity high.
And in the same line of thought here, the urine osmolality is going to be... Increased as well. A little bonus question here. But what is our treatment for SIADH? So our body, again, is going to be really dilute with water.
We're suffering from this dilutional hyponatremia. We need some sodium. So a 3% drip would be fantastic. But remember, we're not correcting it too fast. If we increase our sodium too quick, we could be at risk for that osmotic demyelination syndrome.
We're also going to free water restrict these patients and then place them on safety precautions, both fall and seizure precautions because of that low sodium. Alright, so I completely erased the SIADH column so that we can think through DI here as well. And nobody cheats. Just kidding. So in DI, do we have a lot of ADH or not enough?
If in SIADH we are swimming in ADH, then in DI we're not swimming. We do not have enough. So it's going to be decreased.
And what do we think about our serum osmolality? Well, let's think about it. We don't have enough ADH, which is going to result in water loss.
We are going to be peeing all of the water out because there is no ADH to concentrate that urine. So if we're getting rid of all the water, we are going to be left with a high concentration of solutes in the blood. So our serum osmo and our serum sodium are going to be increased. What about our urine-specific gravity and urine osmolality? They're going to be decreased.
So we're peeing out tons and tons of this dilute urine. It is so dilute that there is going to be a low concentration of solutes there. So we will have a low urine-specific gravity and a low urine osmolality.
And as a little bonus, I'm going to ask the same question here, but what is our treatment for DI? We don't have any ADH, so let's give our body some. We're going to give desmopressin, or DDAVP, which is the synthetic form of ADH. And also, since we've lost so much fluid, we want to replace it so that we don't continue to stay dry and dehydrated.
I do have the two completed charts right next to each other here if you want to look at them. But truthfully, if you memorize one, the other one is going to be the exact opposite. But for me personally, I think it's important to be able to think through both of them. And I hope that my explanation with all of this helped.
Question number 12. You are taking care of a patient in DKA. Six hours after starting an insulin infusion, the patient's blood sugar is 240 milligrams per deciliter and the patient is stable. Which of the following fluids should be administered?
A. 0.45 normal saline with a glucose source. B. Hypotonic saline to provide cellular hydration. C.
0.9 normal saline bolus or D, hypertonic solution to hydrate the cell? The answer here is A, half normal saline with a glucose source. So did you by any chance choose B? a hypotonic saline to provide cellular hydration.
While that is correct, we should be administering that hypotonic saline. However, since our blood glucose is now under 250, we want to make sure that we are also adding a glucose source. So the best answer choice here, not to give you PTSD from the NCLEX, but the best answer choice here is half normal saline, which is a hypotonic solution, but with an added glucose source.
Question number 13. A patient with diabetic ketoacidosis will present with the following. A. Hyperglycemia, hypoosmolality, anion gap acidosis.
B. Hyperglycemia, hypoosmolality, and ketone production. C.
Hyperglycemia, hyperosmolality, and anion gap acidosis. Or D. hyperglycemia, hyperosmolality, and hypernatremia. Thank The answer is C, hyperglycemia, hyperosmolality, and anion gap acidosis.
While we did talk about DKA and HHS separately, I did want to include this table here that compared and contrasted the two. And I did try to bold the ones that I thought were really important. you. So in DKA, you have a positive serum and urine ketones, you have a metabolic acidosis, and the treatment is going to be insulin first. But don't forget about your fluids because they are absolutely hypovolemic.
And in HHS, you are going to have a significant fluid loss of six to nine liters, you are going to have a severely elevated serum osmolality, and the treatment will start with fluids due to the high hypovolemic state, and then will be insulin. Question number 14. What severe complication of hyperglycemic emergencies is also present in diabetes insipidus? A.
Fever, B. Bradycardia, C. Metabolic acidosis, or D. Hypovolemia. I hope nobody got this wrong. I hope you made me proud because the answer is D, hypovolemia. So in both hyperglycemic emergencies, DKA and HHS, you are met with a ton of fluid loss, but also in diabetes insipidus, because remember, they can be losing 6 to 24 liters of urine a day.
So in all three of these, you can absolutely be hypovolemic. dehydrated, and even in hypovolemic shock. Last but certainly not least, question number 15. A patient with SIADH may present with which of the following?
A. Polyuria, B. Seizures, C. Hypertension, or D. Hypernatremia?
What's the answer here? It is B. Why is it B? Because of their severe delusional hyponatremia. Their sodium is so low, they are at risk for seizures, they are at risk for falling.
So make sure, as I'm sure everyone does so well, keep your patients safe. Alright everybody, we have made it to the end. If you liked this video or found it helpful, please like and subscribe to my channel.
I would greatly appreciate it. And let me know if you have any questions. I would be more than happy to help. If anyone is taking their CCRN soon, I hope that you guys have mastered these questions. You can absolutely do this.
You've got this. Good luck to you. Thank you everyone for watching. Nurse Jenny signing off for Nurse Life. Have a good one!