The endocrine system comprises multiple glands (pituitary, thyroid, parathyroid, adrenal cortex, adrenal medulla, pancreas, ovaries, testes, and hypothalamus) that secrete hormones regulating metabolism, stress response, calcium balance, glucose regulation, and reproduction. Common endocrine disorders include hypothyroidism (fatigue, cold intolerance, weight gain, increased TSH, decreased free T4, treated with levothyroxine), hyperthyroidism/Graves disease (heat intolerance, anxiety, weight loss, decreased TSH, increased free T4/T3, treated with methimazole), type 1 and type 2 diabetes (polyuria, polydipsia, weight loss, fasting glucose >126 mg/dL or HbA1c >6.5%, type 1 requires insulin, type 2 responds to metformin), Addison's disease (fatigue, hypotension, hyperpigmentation, decreased cortisol, increased ACTH, decreased sodium, increased potassium, treated with hydrocortisone), Cushing syndrome (central obesity, moon facies, hypertension, increased cortisol, treated with surgical removal), pheochromocytoma (episodic hypertension, palpitations, headache, sweating, elevated plasma metanephrines, treated with alpha blockers and surgery), and primary hyperparathyroidism (stones, bones, groans, increased calcium and PTH, treated with parathyroidectomy). Diagnosis requires matching clinical symptoms with laboratory findings, and treatment selection depends on patient-specific factors including pregnancy status, age, renal function, and comorbidities.
Endocrine and urinary system Q & A FNP/AGNP & AGACNP: Dr. Kehinde Elisha - #fnpstudent #fnp #ancc本站添加:
All right, Dr. Kend Elisha speaking here, founder of MP Certification Academy. Today, we're going to be jumping into endocrine system. Once we're done with this, we're going to move to the next party system according to the schedule. So, what is the content that we're going to be going through to over today for the most part we're going to do an overview of the endocrine system just to bring in the concepts.
It's a lot of concept on the endocrine system. We're going to see how we can remember all of that. And then we're going to be talking about common endocrine disorders, diagnostic tools, pharmacologic management, clinical pearls for MPs and then exam prep Q&A, rapid fire review, test taking strategy and tips for this particular system. So overview of the endocrine system, the gland uh the hormones and the function what are those? So what are the glands that we're going to be dealing with when it comes to endocrine system? It is the pituitary gland. It is the thyroid gland. is the parathyroid gland, the adrenal cortex, the adrenal medadulla, the pancreas, the ovaries, the testes, the hypothalamus and then the problem that can potentially go wrong with each of the gland is also here. Okay. So now this gland right now what hormones do they secrete the pituitary gland act, TSH, GH, LH, FSH, prolactin. It is very very important to know which gland secrete what okay to get to get things straight on the exam. It is important to understand which uh which what secretes what. Does it make sense? Now the thyroid gland secretes T3, T4 and calcetony.
The parathyroid PTSH. The adrena cortex, cortisol, adoststerone, adrenamedulla secrete epine epinephrine or epinephrine. The pancreas will secrete insulin glucagon. The um ovaries and testes secrete estrogen testosterone.
Ipothalamos secret CR, TR, GNR and GHR.
And those all have full definition.
Maybe next time I will have the full definition somewhere here. But I'm sure most of us have experience with this already. Now they each they also have a function as a group. So with the deputy generally what does it do? Regulates other glands. Uh thyroid metabolism, calcium balance, parathyroid will increase serum calcium level. Adrenal cortex will help with stress. you know blood pressure, sodium potassium balance, adrenal medadulla, we do a fight or flight and that's where we have a when you have a problem dysfunction here that is when we start to we tend to have some issues with high blood pressure. What about pancreas uh glucose regulation ovaries and testes will help with reproduction. Hypothalamus is a master regulator that is pretty much the controller like controlling system helps us regulate a lot of things in the body.
So what exactly are the commoner endocrine disorders? When we talk about endocrine system, we are talking about it as a system. We talk about the pieces of it. The part of it in in brief. Now we're now going to say okay those parts things can also go wrong with them. What can potentially go wrong with this part?
We can potentially have hypothyroidism aka aims disease. We can have hyperthyroidism aka Graves disease. We can have diabetes type one. We can have diabetes type two. We can have adysis disease. We can have cushion syndrome.
We can have fiochromosytoma.
We can have which of course you know we just talk about hypertention now. We can have primary paparathyroidism. We can have sadh diabetes incipitus. And then what tools do we need? We're going to be talking about that. But this diseases what exactly are the key things or the key features that we must focus on or that the exam is going to really hold us up to on the exam. That is the clinical feature. A patient comes in with cold intolerance, with constipation, with weight gain. See, now you are now connecting with that on the exam and then you'll be able to know what to pick. So no strategy without content.
Absolutely none. You have to have your content. What are we strategizing without content? So look, hypothyroidism. What exactly is the key symptom? We have fatigue, cold intolerance, constipation, weight gain, brady cardia. Now, every time I talk about something that something is wrong with something or something is wrong with the meds, something is wrong with the body system, there's got to be a lab to monitor. That is our role, right? We got to know what labs to monitor. So, when we have hypothyroidism, what do we see? We're going to see increased CSH, decrease free T4. What about other notes that we need to pay attention to here, which is supposed to be a key concept is um autoimmune, right? Treat with levothyroxine. So we know it's generally an autoimmune. The treatment is also kind of like thrown in here. There's a lot more to consider though for treatment. We have to consider the food drug interaction, the drug drug interaction, the drug disease interaction. We also have to consider the population. But in general, what do we do for hypothyroidism? We we do levothyroxine.
Do we have any questions at this time?
Any questions? All right, please let me know by raising your hand or by dropping a question in the chat. We're now going to move on to the next path though I parathyroidism aka Graves disease. What do we see? Heat intolerance, anxiety, weight loss. So a patient comes in with heat intoler. They won't say withlerance. A patient came in complaining of heat intolerance.
They appear to be anxious or something or they have weight loss. You say what you see and you also go with what patient symptomatology. Pull it all together. That is called the subjective and the objective data and then you come up with the diagnosis. But exam will not like throw hypothyroidism or any of this path on your face. They expect you to pick it up based on the symptom that they present. Right now what labs are we going to be looking for? In fact the exam can also present with this lab on examination or upon um you know reviewing the labs you discover the patient has a decreased TSH increased feed free TT T4 and T3 and they also have TSI. They expect you to be able to connect this with hyper thyroidism or grieves disease. And of course they will not tell you that the patient have hypothyroidism. They will give you this description of symptoms and then they will say how you going to treat it. So let me tell you if you misdiagnose this patient because you don't know what symptom attach or what diagnose attached to this symptom you're going to be picking the wrong drug. But anyway here we know it's hypothyroidism. So we're going to be picking metimazole.
So exam is not going to straight up tell you what diagnosis is. You have to figure it out. So your diagnosis skills is important. Period. So look, diabetes, minitis type one, polyura, polyepsia and weight loss, labs uh and imaging, first blood sugar, anything that is more than 126 is considered of course diabetes, hemoglobin A1 that is more than um uh 6.5%.
NSC peptide will be on the low side. We know it's generally an autoimmune and of course insulin will be required. Type two diabetes militis is often asymptomatic unfortunately. You know what I mean? You just think you're going about your normal life. You have all this obesity and all that. Hemoglobin A1C more than 6.5% fasting blood glucose is more than 126%.
Just the same symptom that we see with type 1 diabetes. All right. But the second type the second type the type the type two though is mostly mostly due to lifestyle and I honestly think genetic also plays a role. So what do we um what do we do? We definitely work on giving some metforming for type two that is a oral anti-diabetic drug. What about Addison's disease? Fatigue, hypotension, eye part pigmentation.
What do we see? Decreased cortisol. We see increased AC. We see decreased sodium level. We see increased potassium. Got to pay attention to that.
Your lab that you're going to see is also a trap for you. They're also going to tell you that the patient comes in with reviewing the lab. You saw increased CAC, you see decreased cortisol, you see decreased sodium. They will describe this lab and pair it with your symptomatology.
Now it's an autoimmune can you can treat it with hydrocortisone.
So now let's go ahead and take a look at Cushing syndrome, central obesity, try atism, hypertension. These are the classic signs of Cushin syndrome.
Increased cortisol, dexamethasone suppression tests um can also be done and of course we have notes here generally too much steroid is the cause of cushion syndrome.
All right. What about fiochromosytoma episodic hypertension palpitations headache sweating?
This is a big deal. Okay. Something that must be picked up.
Episodic hypertension, palpitations, headache and sweating, fiochromoscytoma, what labs do we need? Plasma metanine got to treat with alpha blockers and then surgery. So what about primary hypoparathyroidism, stones, bones, groans, you know, moans? These are pretty much the clinical features that we see. increase calcium, increase PTH, you got to treat with what pretty much having the um part that part you know taken out. So whenever you see ectomy they have to pro they have to perform some kind of procedure to remove that part part SAH hyponetriia and low sodium musality confusion don't worry question is about to come but when questions come and then we are more alert and in tune with this stuff you must have your content ready because those questions you just find yourself guessing on that decrease sodium decrease serum OS increase urine OS It's very common in patients with lung cancer or SS or you know you know very common with lung cancer or SSR. Isn't that crazy? Just think about your SIDH.
A lot of our patients that are actually geriatrics they experience SIDH quite a bit. So hyponetriia is definitely one of the classic symptom or one of the classic side effect uh that we see with the use of SSRI. Diabetes incipidos polyura polyypipssia and of course dilute urine when that when urine is dilute it only makes sense that sodium will go up and then urine also come down right because it's not concentrated now you got to treat with desopress okay now diagnostic tools TSH free T3 T4 you know AC simulation test separation test hemoglobin A1C faster blood sugar o GTT uh PTH, calcium phosphate, urine, metaphor, metaphins, MRI, pediatory, they are the things that we do for all of this concepts. But if you look at it, I linked this test here already. So this is just a reinforcement. Now in general, how do we manage these conditions?
Levothyroxine, what is it used for?
Hypothyroidism. This slide right here, you want to spend time on it if you struggle with form. methazol or PTU hypathyroidism metformin type two diabetes minus insulin type one you know what I mean or type two some type two can get that bad that we need uh insulin as well but for the most part we don't do insulin for type two though we do metformin we do oral medication hydrocortisone or fluocone that's addison's disease desmopressin centradi bisphosphinates osteoporosis sgt2 to inhibitors like empaglphosine type 2 diabetes mittois. What about GLP1 agonist like simaglutine that is very common now for weight loss uh you know it's used for type two diabetes but people actually focus on the weight loss part that they lose sight of what what does it does but let's be careful of this weight loss stuff uh you know what I mean I'm just saying that's me okay so now levothyrosin you want to what are the notes that we must keep in mind take it on empty stomach monitor TSH level methole uh PT in the first trimester only not beyond that because it can be territogenic. Metforming you have to watch out for GI side effects. Lactic acidosis one of the common symptom or things that we see with metforming. What about insulin? Weight gain hypoglycemia are a very common effect of uh insulin.
What about hydrocortisone? Monitor for blood pressure and electrolytes.
Desmopressin monitor sodium level.
Bisphosphinate you want to take with water upright for 30 minutes. SGLT2 inhibitors UTI risk weight loss. What about GLP-1 agonist slows GI emptying avoid in medularary thyroid cancer.
See what I'm saying now? Semaglucide with slow GI emptying. If somebody have a medularary thyroid cancer, they have to avoid it. Now a lot of people are not educated as to when to or not to take these medications.
Now clinical pros for all MPs TSH is most sensitive test for thyroid function. Your TSH level is your thyroid function is off. TSH level is one of the gold standard that we want to obtain to ensure that we nailed the right diagnosis.
Then always re check labs before adjusting thyroid meds. Avoid metformin.
If the EGFR is less than 30, we don't want to take things further down. Check cortisol every morning. Weight loss with good appetite. You think hypothyroidism.
Pregnant women use PTU in the first trimester, then switch to methos. Beta blockers help control adrenic symptoms in hypothyroidism.
So, we're now going to go through some of the exam style questions. The way I have them though, I think I have it as let's go through it as it's too late anyway to take out the answers. Let's go through it as a simulation. I think that's the way I had it this way. So meaning what we're going to go through this question. We're going to tear it apart. We're going to study the question. Okay? So this is for learning purposes only. This is not for oh give me the answer. I don't care about the answer. I want you to be able to actually understand how to read questions and answers. So let's take a look at the first one. A 34 year old woman presents with weight loss, power mutations, heat intolerance, TSH is low, T4 is elevated. What is the most appropriate firstline medication? A levothyroxine, B methosol, C proponol, D ptu. So now let's look at how to read this question.
A 34 year old is a keyword. woman is a keyword. Weight loss is a major keyword because it's going to also direct where to go or direct us on where to go.
Palputations, heat intolerance automatically.
You have to come up with a diagnosis here. What is your diagnosis automatically? Okay, it's going to help you out. What is your diagnosis here?
Forget about the answer.
Drop your answers in the chat. What is your diagnosis for this patient?
Let's go back to the content.
What do we see here? Eat intolerance, anxiety, weight loss. What is hyperathyroidism?
Grave disease. Okay. So now let me say you pick out pick that out in your mind.
This is what I'm saying. Now you pick it out in your mind. Okay. Exam is not saying that it is. You will now have the ability to match it up with the right treatment. That is the way it works. No strategy without content. Absolutely none.
Do you get it now? So we know the answer is methosole. Let's take a look back at the content. It says right here, methosol is used for hypothyroidism.
The key symptom it says right here, hypothyroidism symptoms, it intolerance, anxiety, weight loss, and tremor. Do we get it?
All right. Now, let's keep it moving to the next question. You see how I put thyroidism is a trap. So, you can't go into that exam thinking, "Oh, I'm I'm not sure." No, you got to be sure. Your diagnosis is a big deal. And on in our confident prescriber group, we actually have a separate class for diagnosis alone for all specialties, FMP, AGMP, PMHMP.
You know, diagnosis is something that must be learned. Diagnosis is what will take you to another level. If you can't diagnose, what are we treating? But a lot of students worry a lot about, oh, I want to know my farm. And that's good to know your farm. But if you don't know what if your diagnosis is wrong, most likely your pick is going to be wrong, too. Question two, a 42 year old keyword. If you know your keyword, throw it in. old man right with type two diabetes has an A1C of 88.2%.
He is overweight and unmet for me. What is the next best step? What is the next best step? Add basil insulin. Add SGLT GLT2 inhibitor. Switch to soponura.
Increase metforming.
So we are not here to look for answers.
We're here to look for okay, how am I supposed to think correctly on the exam?
How am I supposed to see the right answer here? A 45 year old man with type 2 diabetes has an A1C of 8.2%.
He is overweight. I'm like, "Oh my god, it sounds like really bad." Type two, A1C more than 6.5.
That's okay. He's overweight and he's on metforming already. So, this is not even touching him. Okay. So, it's time to do something different. It's time to add something else for more efficacy and that is why we are picking what? SGLT2 inhibitor. Now this is according to guideline. B final answer. SGLT2 inhibitors like empaglyphloine help with weight and CV risk.
That is important to this for this patient at this time because what we said the patient is having that type two diabetes A1C is not going down on me for me already. We know that something is something's got to be done fast to get the blood sugar down. B final answer right that is pretty much that. So what is the purse for the endocrine system?
Your your diagnosis is B is a big deal.
What is your clue for each of these symptoms?
When you see on your exam, when you see weight gain, code intolerance, you're going to be thinking right away, what hypothyroidism.
When you see it intolerance and anxiety, you're going to be seeing hyperthyroidism.
Bronzekin hypotension, you're going to be suspecting Addison's disease.
Moonface and Stri, you're going to be suspecting Cushin's disease. stones, bones, and groans, you're going to be suspecting hyparathyroidism.
When you see keywords like high urine output, low specific gravity, you're going to be suspecting diabetes incipidos. When you see hypertension plus palpitations plus headache, you're going to be seeing what? You're going to be suspecting focyto.
All right. Now, let's go ahead and talk about test taking strategy tips. Always match symptoms with labs. Know the drug.
Uh when when it comes to blackbox warnings, know when not to give it. You know, um when in doubt with thyroid, you want to check TSH first. Reproductive age of a woman, you want to consider pregnancy complications for meds. For fatigue, hyponetriia plus hyponetriia, you better be thinking Addison's or SIADH.
for weight gain plus buffer low hump.
You better start thinking of Cushions disease.
So now we have that was a preview. Okay.
And you're like well I thought we're done. No we're not. We're just getting started.
Let's now go through some of the advanced concept.
We're going to go through endocquin disorders overview symptoms and labs. A lot of them overlap anyways. Uh what we do for anklas is also what we do for advanc. It's just that advanced your roles will now play a role. That's the difference. But it's still the same body system. Does it make sense? Clinical thinking question endocrine system common assessment tools. Now that is now your advanced role. Does it make sense?
Um pharmacology of endocrine system. Um then multiplechoice questions, answers, test taking strategies and so on. Okay.
So now we're not going to go over the advanced. Honest there's nothing advanced about it. Let's be honest here too. But we are now talking about first line, second line and all that stuff though for type two diabetes. We already know what it is. We learned it in the basics already. We went through the basics first. So what is the first line?
Lifestyle modification plus metforming.
Type 1 diabetes. What is the first line?
Insulin therapy, hypothyroidism, levothyroxine, paripathyroidism, methos or beta blockers. Okay, that is kind of the only thing that is different. the labs we went over why why though why behind the labs is also something that we didn't really go over but it only makes sense when something is off then you go for that lab so it's just about it's just about knowing what is off and dealing with what is off knowing what the problem is and fixing the problem aim thyroiditis you want to treat with levoth thyroxine right Graves disease methos how will you remember this it is nonnemonic necessary pneummonic is extra work. I have pneumonics for all of this. The best way I found out to learn this is repetition, repetition, repetition.
Hypoparathyroidism, parathyroid, uh par thyroidctomy or monitoring plus hydration, hypoparathyroidism, calcium plus vitamin D supplementation, vitamin D deficiency, vitamin D3 supplementation.
Okay. So these are things that we do for these common conditions. Osteoporosis, bisphosphinate.
Okay. The things that we have not seen, I'm going to quickly talk about them. We have not seen osteoporosis.
Don't forget dexa scan, calcium 25, hydroxy, vitamin D, TSH are things labs that we're going to obtain. Why do we need this lab? To see what our bone density is. Is it low? to rule out any kind of secondary causes and bisphosphonates plus vi calcium or vitamin D is the main treatment for osteoporosis.
What about metabolic syndrome lifestyle modification? You want to be able to assess cardiovascular or metabolic risk.
What about obesity? Of course, we know that we're getting weight gain, sleep apnnea, joints start to hurt and stuff like that. The best force line treatment is still diet and exercise and of course behavioral therapy, controlling our mind and controlling what we put in our mouth. Pickles is a big deal too when we have irregular menes, acne, obesity.
But exactly what labs do we need though?
Testosterone LH or FSH ratio ratio bic ultrasound fasting glucose. We're also going to diagnose picles and rule out other causes of androgen excess. as the focus of this workout uh of this uh process. OCP, lifestyle, metforming are the things uh that we can potentially use as a first line treatment. And then we have adrenal insufficiency. What are the symptoms of adrenal insufficiency?
Fatigue, hypotension, you know, weight loss, eye pigmentation, you know, what labs do we what labs do we need to order? AM cortisol, ACT, electrolytes, sodium, potassium. Why do we need this lab to confirm cortisone deficiency and the type? What is the first line? The first line is hydrocortisone or prednisone. Excuse me. Now cushion syndrome moon phase. We saw this earlier under the when we did the the foundation central obesity purpose try and muscle weakness. What lab do we need to order here? 24-hour urine cortisol dexamethasone suppression test. And why do we need this lab to confirm cortisol excess? What is the first line treatment then? Surgical removal of the tumor and then we have to taper the steroids if we have them on there. We don't stop steroids abruptly. Fiochromoscytoma what are the symptoms that we see?
Paroxyma hypertension you know palpitations sweating headache.
These are things we see with focytoma.
Plasma metaninephrines 24-hour urine kakolamines are things uh that we need to order to rule out focytoma.
We want to confirm katakolamine or secretreting secretreting tumor because you got to because other things can also have the symptom. When we do this test, it's going to help us nail whether it's is truly focytoma or not. So what is the solution to the what is the end game?
End game is adrenalctomy. They have to surgically remove the tumor. What about IPA aldostroneism, hypertension, hypocalemia, fatigue are things that we see. Plasma adoststerone, running activity, electrolytes. You want to assess for primary adostism.
spiralactone or surgery are things uh that we need to end uh we need to use to treat um hyperadostrinism then we have hypogonadism that is in men we have menopause in women we have prolactinoma we have sih diabetes and incipidos we're going to go through each of them with hypogonadism what do we see that means somebody have a low lipido they have erectile dysfunction decreased muscle mass you know And of course total to testosterone uh le LH FSH are the labs that we're going to draw to rule out uh this condition. But why do we need it? Of course we have to confirm because other things also carry this symptom. What is the first line though?
Testosterone replacement if appropriate.
With menopause we see hot flashes, night sweat, vaginal dryness, uh mood swings.
So what labs do we need? Follicle stimulating or moon estradio. Why is that? confirm to confirm an opposer status. Uh what is the first line? HRT if no contraindications. SSRIs for vasom model symptoms. So we treat what we see.
You look for the cause and treat the cause. What about prolactinmia, galactoia, amenoria, fertility, visual changes are things that we see. Serum prolactin, MRI, pituitary are the labs that we need to draw for this patient.
What about pro diagnose pituitary tumor?
Why is that? That's why we, you know, we rule it out because if you don't diagnose pitary tumor with this work up, galactoia can also come with other things. It can even come with something as small as our antis anti- um psychotics, you know, can cause galactoia. A minora can be caused by so many medications, infertility, anything can cause that. Visual changes, many meds can actually cause that. So we need to rule out that this is truly uh prolactinoma.
So we have to obtain the lab prolactin.
We have to do MRI of the pituitary gland. What how do we when we confirm it? What do we fix it with? Dopamine agonist like sebagoline. Sih also is the next one. Hyponetriia confusion fatigue is what we see with SIDH. What labs do we need to obtain? Serum sodium serum osmolity or urine osmolity urine sodium why is that we need to diagnose the cause of dilution hyponetriia fluid retention treat underlying cause now we're going to quickly go next to the next slide diabetes incipitus polyura polyypsia and dilute urine is what we see with diabetes incipitus with diabetes you peeing a lot right now so what labs do we need though serum sodium serum osmol mality, urine osmolality, water deprivation. Now, these all have values and ranges to go with them, but we're not getting into that right now.
We're just going straight to okay, what labs do we need? At least build that foundation, then then then you advance.
So, why do we need it? Of course, to make sure that we're not mixing up central and nephroenic together. So, we need to see what the cause is and treat the cause. If we do establish that this is in fact diabetes, what do we need to treat it with desimressin thioide these are things we're going to use again depending on the cause of it.
If it's a central diabetes incipitus you use desopressin if it's nephrogenic diabetes incipitus you use thioides. All right and that is pretty much it. So now advanced content here when we see diabetes incipidus, diabetes militus, hypothyroidism, other things also look like it. When we say other things look like it, that is now the differential diagnosis. So with type two diabetes means what else look like it? The closest is type 1 diabetes.
Does it make sense? And of course the money to remember is too much insulin resistance and stuff like that. What about type one? The closest is type two.
It is important to know where your differential is. It is important to know what else is close to it. All right, we're going to take a quick question here before we proceed. Any questions?
Right here. So, this is an advanced content. When you when you start talking about differential, you are thinking about okay, what else is close to this? That way your confusion is less. So, differential diagnosis have its own really relevance, right? Hypothyroidism is close to depression. Hypathyroidism is close to anxiety. Ashimoto thyroiditis is close to hypothyroidism, the non-autoimmune one. Graves disease is close to other other hypathyroid disorders.
Hypoparathyroidism is close to malignancy related hypocalcemia.
Hypoparathyroidism is close to vitamin D deficiency. Vitamin D deficiency is close to hypoparathyroidism. It only makes sense. Osteoporosis is close to osteom mallaysia. Metabolic syndrome is close to diabetes, diabetes, type two diabetes. Obesity is close to cushion syndrome. It looks like it by the time your face is round and stuff like that, right? Picos will look like non-classic cah. So irregular period ceased and all that. So periods come occasionally and you know and go. But they also have issues with child birth unfortunately.
Now adrenaline insufficiency is close to hypothyroidism.
Cushion syndrome is close to metabolic syndrome.
See obesity is close to cushion syndrome. Cushion syndrome is close to metabolic syndrome. Metabolic syndrome is similar to obesity. It's the same as obesity. Can you see how they all cross crisscross? Fiochromosyto is close to panic attack. The way it shows the way it presents itself. Hyper hyperadro adro aldostrinism is close to essential hypertension. Hypogonadism is close to depression or hypothyroidism.
Menopause is close to hypoparathyroidism or depression. Prolactinoma is close to hypothyroidism or pregnancy. SADH is close to hypothyroidism and addison.
Diabetes and cypus is close to psychoggenic polyypsia.
And that is it for the endocrine system.
We're now going to dive right into Q&A.
Are we ready for this? Please drop your answers in if you know it. To 24 year old underweight female present with fatigue, weight loss, frequent urination and fasting blood sugar is 280 mg per DL. Lab shows C peptide levels. What is the most likely diagnos? And what lab confirms it? That is double double dip right there. A type two diabetes. B conf uh confirmed by I mean sorry A type two diabetes confirmed by fasting glucose. B type 1 diabetes confirmed by low ceptide. C metabolic syndrome confirmed by insulin resistance. D type 2 diabetes confirmed by elevated A1C. What do we think? Providers. So much for your responses. I got enough response in the chat now. So we're going to keep it moving. Type 1 diabetes confirmed by fasting fasting glucose.
Why is that wrong?
If you Okay, let's let's not start.
Let's not approach it this way. Let's approach it this way. Put the two wrong answers that is likely wrong. Put the two wrong answers in the chat.
The two wrong answers. This one, this one was not difficult anyway. So, I really think we should be able to get through this one really fast.
So we know the final answer here for sure um is B. Okay. But if you have to pick two wrong answer, A is out and D is out. Those are two obviously wrong ones.
Okay.
Type two diabetes confirmed by fing blood sugar. Uh type two diabetes. You want to remove those two. They parallel together anyways. there's an opportunity to just knock those two out and you have to worry about okay it's probably C or B or C and now you can just definitely see okay weight loss fatigue and they said blood sugar and they said underweight female present with fatigue and urination and then C peptide levels is your major clue right there C peptide levels and that would connect you with type 1 diabetes B final answer okay now let's look at the rationale rationale look at it type 1 diabetes This is an autoimmune condition with destruction of pancre pancreatic better cells resulting in little to no insulin production.
Cepttide is a byproduct of insulin production. A low level confirms insulin deficiency pointing to type 1 diabetes.
So your major clue is the ceptide. Type one rule out with C peptide. Type one you want to rule out with C peptide. So the patient is young underweight as a classic of type one diabetes making is the best feed. Now type two confirmed by fasting glucose is incorrect because fasting glucose while fasting glucose is more than 126 support diagnosis of diabetes it does not distinguish between type one and type two. So type two usually is seen in overweight uh of course uh insulin resistant adults uh the patient is underweight that is a major rule out that's why we rule out A and D okay and of course metabolic syndrome is confirmed by insulin confirmed by insulin restant is wrong uh because it includes central obesity uh high triglycerides low HDL hypertension elevated fasting glucose patient does not show these features no insulin resistant tested or mentioned in the case now don't reading into the question, focus on what exactly they're asking you. You want to say, okay, what exactly are they asking me? Type two diabetes is confirmed uh by hemoglobin A1C. He emoglobin is incorrect because emoglobin A1 supposed to confirm the presence of diabetes but cannot distinguish what the type of diabetes that you got. Uh this patient's clinical feature is more consistent with type 1 diabetes. Thank you so much for your participation. Speaking is Dr. Kind Elisha, founder and CEO of MP Certification Academy. The next thing we're now going to go uh go to is question number two. Case number two. A 45year-old woman presents with fatigue, cold intolerance, uh weight gain. She has been taking SSRIs for depression with minimal improvement. Question. What tests or which test should be ordered to rule out metabolic cause? A. Cortisol. B LH or FSH C. TSH and free T4. D.
Emogloin A1C. What do we think?
Please drop your answers in.
This is pretty straightforward, right?
What is your diagnosis?
Diagnose first.
If you diagnose first based on this, you and I will agree that this is what hypo thyroidism.
So if it's hypothyroid is a module we see we say increase TSH level right so TSH is one of the things we're going to work on that will be our clue C final answer okay so content is still key here the ability to diagnose is a big deal on this test you have to know your diagnosis so let's take a look at the rationale hypothyroidism commonly mimics depression TSH thyroid stimulating hormone and free T4 are the best initial test to evaluate thyroid function elevated TSH with load free uh free T4 confirms primary hypothyroidism.
Now with cortisol it's incorrect mainly because it is a test that we use for adrenal function like Addison's disease or Cushian's disease um not the very first line for evaluating fatigue or depression like symptoms. LH or FSH is incorrect. Uh because it evaluates Canada or menoposa status. Uh this does not com um this does this does not explain cold intolerance and weight gain. Hemoglobin A1C is used to diagnose or monitor diabetes not fatigue or cold intolerance.
So C final answer. Let's look at the third case. It's a 34 year old female. A 34 year old female is a key word present with palpitations in eat intolerance this time weight loss this time and exofothalamus which lab and physical finding confirmed the endocrine diagnosis a TSI antibbody and exofothalamus B TSH and mood swings Cogmoglobin A1C and palpitations D free T3 and tachicardia drop your answers in the chat Okay, I'm just spelling that out, but it is in fact the final answer. It is thyroid antibbody, thyroid stimul, thyro stimulating hormone antibbody and exothalamos.
But what are we thinking when we saw this question though?
Is it hypothyroidism or is he hyper thyroidism?
Let's diagnose this first.
Don't forget this is Graves disease hyper thyroidism.
And that kind of led us to a final answer. So thyroid stimulating uh imunoglobin um confirms autoimmune hyperathyroidism aka graves disease exothalamus that's the bulging of the eye I remember that high in the biology book is pathogenomic for graves disease not seen in simple anxiety TSH and mood swings TSH may be low in hypothyroidism but mood swings are nonspecific and could occur in anxiety or other conditions.
It doesn't clinch the diagnosis.
Hemoglobin A1C and palpitations is incorrect because hemoglobin A1C assess glucose not thyroid palpitations are nonspecific and seen in both anxiety and hypothyroidism.
free T3 and tachicardia uh is incorrect because while free while free T3 is elevated in hypothyroidism ticardia is also seen in anxiety without a more specific sign like exothalamus or TSI this is not enough to confirm the diagnosis okay let's take a look at another question here's a 38-year-old woman 38y old woman key word present with weight gain weight gain key word of course is he bruising is a bruising keyword word popular abdominal stride.
Popular abdominal stride is keyword and then uh she also reports new onset of hypertension which which of the following is the most appropriate initial lab to confirm the suspected diagnosis? A emoglobin A1C B TSH and free T4 C dexamethasone suppression test D serum creatine. What do we think?
Abdomen try with gain is a bruising round face.
What are you suspecting?
What is Cushin's disease?
Okay, now that we have that in order, what is now going to we now it's easy for us to pick an answer the exam suppression test.
C final answer we know it's not hemoglobin A1 it's not TSH we saw with the relevance of this just now we know it's not serum creatine that's about a kidney so dexamethasone suppression test confirms cortisol over production seen in cushions first line for diagnosing IP cortisolism now you only know that this is cortisololism wait a minute that's a cortisol yeah which is of course cushions too much cortisol will lead to cushions okay IP cortisolism will lead to cushions Okay. So now, so C is the final answer. Emoglobin A1C is wrong because may be elevated in cushions but is not diagnostic. It does not confirm cortisol excess. TSH and free T4 evaluate thyroid function unrelated to two moon phase or stri serum creatine may may assess kidney function but is not relevant to diagnosing questions.
Let's look at case number five. is a 62 year old man woman present with bone pain, fatigue and kidney stones. Lab review reveals elevated calcium and elevated um parathyroid which was which what is the most likely cause of hypercalcemia?
A multiple myoma. B primary hyp parathyroidism D uh C vitamin D toxicity D hyper parathyroidism.
There is primary hyparathyroidism and there is parathyroid. So don't mix those two up. What will you likely eliminate first? What is the main thing you want to eliminate first?
This is not telling us anything about multiple myoma and C is out. I'm going to suspect B and D. Right. Thank you so much for your responses and I'm seeing a lot of people actually getting the answer right. The final answer that makes sense going to be B. Primary aparathyroidism.
Okay. And primary aparathyroidism is cotized by what? Elevated calcium and PTSH.
I mean PTH. Sorry about that.
And that's a classic sign. What is incorrect? Multiple myoma can cause hypercalcemia but would show slow low PTH due to suppression. Vitamin detoxicity causes high calcium but typically low PTH PTH.
Hypoparathyroidism causes low calcium not elevated calcium level. Okay, so we got more questions. That is pretty much the last one that was left actually and then you can do that on your own. You have access to it. We're now going to go to clinical assessment tools.
Okay. History and physical exam.
Identify symptoms like fatigue, weight changes, hair loss. What about growth charts for pediatrics? Want to evaluate shorts? Are they shorts? Do they have early puberty? Uh do they have thyroid and gland issues? Uh BMI calculation.
You want to assess do they have obesity?
Any metabolic syndrome? What is the waist circumference? Can you detect any kind of central obesity? a marker for metabolic syndrome. What about blood pressure monitoring? Hypertension may suggest cushions for chromosyoma or hyperdostroneism.
What about visual field testing? Screens for uh bmporopsia and pitury tumors. What about skin impact inspection? Looks for hyperpigmentation, vitiligos, dry dry skin, Addison, cushions, pickles and hypothyroidism.
You want to inspect skin for all of that. What about the labs? This is now repeating. You will now see that things are repeating, right? So for thyroid disorders, TSH free T4, free T3 are the common labs that we order. For diabetes, diagnosis and monitoring, immoglobin A1C, fasting glucose, O GTT is what we order. Now, differentiation between type one and type two is mainly C peptide.
With C peptide is associated with type 1 diabetes. What about autoimmune disorder is low in type 1 diabetes? It can be normal or in type two. So it's not specific for type two. Okay. Now with um autoimmune thyroid disease um gra um the anti-TPO and TS antibodies is used for Graves disease. What about the PTH calcium phosphate? We use that for parathyroid disorders. ACT cortisol we use that for adrenal insufficiency and cushion syndrome. Reno and adostronism, adostone levels which we look we use it for hyperadostroneism.
Prolactin pitutary adrenomomas adenomas testosterone LH FSH we use for hypoconadism picos and menopause.
Vitamin D we use for bone health secondary hypoparathyroidism.
Urine catakolamines plasma meta metaphin metanphins we use for fiochromoscytoma.
What about imaging neck ultrasound? We may be trying to look for like thyroid nodules or go for dexa scan. It assesses bone mineral density. MRI of the pituitary will evaluate adenomas or masses like prolactinoma. CTMRI or adrenal glands assess adrenal tumors you know cushions of fiochromosytoma.
Pelvic ultrasound detect ovarian cysts.
X-rays will um you know detect bone uh age assessment for growth delays and that is it. So now we have some cases to follow similar to the case this one is just about test and procedures test and procedures test and procedures. So ensure that you take a look at those questions and make sure you you know check them out play through them try to understand how the examining body is going to ask you questions on test and procedures. Then we have the pharmacology of the endocrine system. We spoke about a few of them before but we're going to talk about a little bit more now and in a little bit more depth.
We're going to be talking about the mechanism and the clinical rational for actually choosing this drug. So why do we give levothyroxine for hypothyroidism? First of all, what is the mechanism of action? Uh you know synthetic T4 convert to active T3 in the body. It mimics a natural hormone is the main reason why we choose it. It is well tolerated and is predict and it's a predictable dosing. Methazol methole is used for hypothyroidism. It inhibitates thyroid what? Perodix peroxidase blocks T3 or T4 synthesis. But why do we choose it though? Because it has fewer liver side effects versus the PTU.
PTU is also an option. But methimazu has fewer side effect. Cuz they will also ask you on exam why you're choosing what you're choosing. They want to test your knowledge that you actually know what you what what you what you know that you're just not doing guess work. Now protu is used for hypothyroidism in pregnancy in pregnant folks during the first trimester.
What is the mechanism of action? It inhibits thyroid hormone synthesis and of course T4 to 23 conversion. Why do we choose it? Chosen early in pregnancy. It is lessenic than methosole. Methmos is not ideal for somebody that is pregnant.
Uh that is why we choose PTU for pregnant moms. Now PTU is not really really efficacious like methmos but we can use methosole in general population for hypothyroidism.
Now let's talk about insulin. Type one and type two diabetes is what we use insulin for. It can be ideally it's for type one. Right now when we have resistant type two treatments to metforming for example we're going to shift gears to you know type one. So what is the mechanism of action? It replaces endogenous insulin. It lowers glucose. Why do we why are we choosing insulin required in type one for sure that's the only thing that we can do. Uh that's the main thing that we can do and it's also used in oralo agents when oralo agents fail or during acute illness. Metformuinide is used for type two diabetes. It can decrease uh epatic glucose production.
Uh increase insulin sensitivity. What is the first line for type two diabetes? No weight. It is the first line. It's good for first line. Metform is good for first line for type two diabetes.
Mettosis. And of course um you don't gain weight while on it. And of course um you don't drop your blood sugar too fast. Just like ins with insulin you can drop your blood sugar way too fast. What about GLP1 agonist like simaglutide lauraglutide the use for type two diabetes and obesity as well. What is the mechanism of action? It actually mimic inrectin it increases insulin it decreases glucagon and it decreases your appetite. So you don't eat as much. So we think food is a sort of weight gain all the time. I kind of disagree with that. Some weight gain is just sedentary like you just don't move enough and most of us are just like that in healthcare. Uh so food is maybe a part of it too because you can cut down and tone down what you eat at least right to make up for the times that you don't move but it still wouldn't match but if you realize by the time you start moving it kind of works hand in hand with the diet. So why are we choosing DLP1 agonist like semaglutide and lautide? It promotes weight loss, low hypoglycemia and cardiovascular benefit.
What about SGLT2 inhibitors like empaglyphloin? It's used for type 2 diabetes, heart failure. It can block glucose reabsorption in the kidneys. It will increase urine glucose excretion.
So why are we choosing it? Because it will improve blood glucose, will help with weight and it also reduce cardiovascular risk and renal risk.
Sulonurus like glucoside is used for type two diabetes. What is the mechanism of action? It stimulates insulin release from pancreas. It is cheap but risk of hypo hypoglycemia and weight gain. What about thazol zones like we call it ties easy to pronounce. You don't have to pluck your teeth over that is for type 2 diabetes. uh you know and of course it is uh you know increase insulin sensitivity in muscle and fat extremely good for insulin resistance but uh you know risk fluid retention though and fractures that is the downside of TZDs what about calcium and vitamin D uh we use for osteoporosis ipoparathyroidism I always emphasize my thyroid whether it's IPA or ipo because we can't mix those two up. What is the mechanism of action of calcium and vitamin D supplement for bone mineral mineralization and PTS PTH support? So why are we choosing it? Prevent and treat bone loss and support calcium or homeostasis.
What about bisphosphinates like adendronate is used for osteoporosis.
What is the mechanism of action? It inhibit osteoclast bone resorption.
Right? Now why we why why are we choosing it? It is the very first line for bone loss prevention especially postmenopausal women. What about synalet I parathyroidism especially secondary and of course the mechanism of action is that it increases calcium sensitivity of parathyroid and it decreases PTH in return. So it is used in CKD or non-surgical candidates. That's why we choose it. What about IP um what about hydrocortisone or prednizone? Whenever we have adrenal insufficiency, this treatment is very ideal. Adrenal insufficiency aka Addison's disease. Now for every pathology, make sure you also know the second name. It replaces cortisol or anti-inflammatory and metabolic effect. Why are we choosing it though? Why do we choose hydrocortisone or predisone? Because it's needed to prevent what adrena crisis. We don't want to throw patients into that. That is not a good thing. And it mimics kicadian rhythm as well. That's why we choose it.
Flutrocortisone. That one is used for adance disease as well. It's a mineral cortical replacement and of course it acts like adoster sodium retention potassium excretion uh you know that that cascade help maintain blood pressure and fluid balance right in the adrenal ins uh you know in a patient with adrenal insufficiency.
Now what about uh cabagoline prolactinoma? It's a dopamine agonist.
Don't forget you cannot say agonist when you mean to say antagonist. You cannot say antagonist when you mean to say agonist. Agonist we're giving it to them. Antagonist were blocking it. So this dopamine agonist they are getting it right. Inhibits prolactin secretion.
They work in opposite ways. Okay. Now what about why choose it? It shrinks tumors, restores fertility and oral dosing. What about desopress?
Desmopressin central diabetes and cypus.
Uh synthetic uh ADHD ADH increases renal water resorption and then prevents polyura and dehydration in ADH deficiency. What about spiralactone?
Hyperdostroneism picos. Okay. What is the mechanism of spirolactone?
Adostone antagonist. see aldoststerone antagonist and therefore a potassium sparing diuretic. Does it make sense now? Aoststerone antagonist. So it's a potassium sparing diuretic. So why are we going to why are we choosing it?
Because it's going to help manage hypertension. It's going to decrease androgens in picos and it's going to protect um protect uh K+ which is going to be pretty much uh it's not really protect K+ that would be a wrong use of word really.
Okay. The right use of words will be it's going to spare potassium.
It's going to keep potassium from going out of the body. So we're not going to be losing potassium but at the same time potassium can then build up and create problems too. So we just have to maintain a balance.
So key decision making factors for NPS patient specific factors pregnancy age renal function test causeities. These are how we're going to pick medication.
How do you select medication? Just don't pick just to pick as well on your exam.
Look at the entire look at the big picture before you pick a medication.
Side effect profile. Risk of hypoglycemia, sulfonurius, weight gain or fluid retention. Evidence based guidelines ADA, AAC, ATA, CANMAT and others guide uh first line firstline choices, insurance coverage, access to care and all that would determine what you pick.
Let's take a look at this question. A 55year-old man with newly diagnosed type 2 diabetes has a mllovin A1C of 7.81%.
He is overweight and has no contra indications. What is the best initial medication? A insulin B metform C.
Sophonur D G glp1 receptor agonist. Drop your answer in the chat. Providers see multiple answers in the chat. I'm seeing just one answer in the chat. We've said it many many times. Type two diabetes oral is always the best. This person has no contraindication to this drug. They have no we don't have to worry about lactic acidosis or anything. In the final answer is going to be metforming.
Metform is the very first line due to efficacy, weight neutrality, cardiovascular benefit and low hypoglycemia risk. Insulin is reserved for severe hypoglycemia or failure of oral agent. So our first line for type two is definitely oral.
Our first line for type one is definitely insulin. See now when we have resistant type one to type two treatment then we go to insulin but we don't jump right on into insulin first. Sulfonur like glucoside if it's effective but higher risk of hypoglycemia and weight gain generally second line after metforming. GLP1 receptor agonist uh you know often used uh after metforming or in patients needing weight loss or cardiovascular risk reduction not the initial therapy. Let's take a look at question number two. All right.
Question number two is a pregnant woman in her first trimester is diagnosed with Graves disease.
Which anti thyroid medication is preferred? A. Methmos. B. PTU. C.
Radioactive iodine. D. Beta blocker.
Approach this question this way. Keyword pregnant woman at first trimester diagnosed with grave disease. Now pick out the population because it's important. What we pick for this woman is going to be important. We just went over it in content. I'm expecting a 100% answer providers guys 100%. Now remember we're talking about PTU not being the best efficacy wise but because this woman is pregnant we're shifting to that. Now if you don't have pregnant woman in your question tell me how will you treat this patient.
Let me say you don't have a pregnant woman there. What will you pick? What is your priority pick without a pregnant woman? You're going to pick methole if there is no pregnant woman story there because methole is actually more efficacious. But we skip it and jump right on PTU because this woman is pregnant. Methazol have a high what?
Terattogenicity.
We're not going to flip through rational and see what it is. PTU is preferred 100% everybody due to lower terattogenic risk. Switch to methazone later when the baby already formed. Right now, methimas risk of terattogenicity in the first trimester you want to avoid initially.
Radioactive iodine is contraindicated in pregnancy due to ferothyroid damage beta blockers alone symptomatic control only does not treat the underlying disease.
Question number three is a 62-year-old postmenoposa woman as osteoporosis diagnosed with dexa scan. Which medication is the very first line to reduce the fracture risk? Calcium supplements alone bisphosphinate aka alandrrenate uh not aka example alandrinate that belong to that class estrogen therapy decalcetony what do we think participation absolutely we're not the finance size bis phosphonate is the very first line therapy in inhibits bone resorption and of course reduces fracture risk you know calcium supplements alone will not help it's important but it's not enough Okay, so we're now going to shift gears and go to question number four. A patient diagnosed with Addison's disease requires hormone replacement. Which drug replaces glucocortical deficiency? Will you remember this? A flu cortisone, B hydrocortisone, C. Predinazone, Dextoone. Do you now see the reason behind uh the foundation that we did?
Drop your answers in the chat.
And when we look at Addison's disease, absolutely absolutely thank you so much for your responses. Uh the final answer is glucocortical replacement that mimics the natural cortisol. Fluocortisone is a mineral cortical replacement does not replace cortisol. Prednazone is used uh but hydrocortisone is preferred because shorter half of life and physiological effect. Dexamethasone is a potent glucocorticoid uh and of course it lacks mineral corticoid activity and longer halflife.
It is less physiologic. Okay. So we have a few more questions here that you can do. Okay. Make sure you finish the rest.
But let's now look at the test taking strategy. So what is the strategy to approach this particular body system or most of the body systems? You want to read this term very very carefully.
Identify the key symptoms first. labs and patient contest. I will add to this one and diagnose. When you identify symptom, whenever it's possible for you to diagnose, diagnose and then take that diagnosis to to your answer. What I'm saying? So, you have to you have to be able to diagnose. It's not a choice.
Endocrine disorders often have overlapping symptoms. Details matter.
The age also matters. It's going to also help you differentiate things. Identify the main clinical problem. Is it IPO or is it hyper? Is it related to a specific gland? Connecting these dots is also a testing strategy. Narrow down the possible endocrine disorders early. Note any lab value provided. Look for patterns. Is it elevated TSH? Is it low free T4? Is it parathyroid?
Hypothyroidism. Is he calcium? Is he hyperarathyroidism?
You know labs often clinch the diagnosis. Understand normal ranges and hormone feedback loops. You want to use pneumonic if you have it if you if you want to use it. for me is not it's an additional study for me but if you like pneumonics please go for it you know bones tones groans and moans for hyper pararathyroidism you know it just kind of help you remember the symptoms that you see with hyper pararathyroidism it's going to help you recall the associated signs and symptom consider patient specific factors are they pregnant what is their age what is that comorbid condition any contraindication some drugs like PTE versus what methosol in pregnancy or diagnosis of Type one versus type two would depend on patient factors. What about prioritize first line treatment? Absolutely. No guideline preferred medications like metform is the first line for type two diabetes.
Levothyroxin is the force is is the is the force for um you know hypothyroidism. So many question will focus on standard of care management and clinical guidelines too. Now you got to watch for distractors though. You want to eliminate options that are outdated, overly broad or unrelated to endocrine physiology. Many options may seem plausible. You want to narrow down by relevance. What about analyze drug mechanism when pharmacology is tested?
Match drug actions with pathophysiology like GLP1 agonist increase insulin secretion and promote weight loss. You want to understand mechanisms uh mechanism help rule out uh wrong choices that you know want to manage time effectively. Don't spend too much time on a single question. You want to flag and return if needed. You want to ensure uh to get all questions in the same or in the exam. You want to make sure you get to it. You want to touch up on everything. Know your lab and interpretation. Differentiate similar presentations. Recall. Remember I tell you that when you have similar presentation, it's going to throw you off on the exam. For example, hypothyroidism versus depression. You must be able to separate that too.
Recall side effect of endocrine drugs.
Help answers questions you know about contra indications and patient educations or patient education. You want to practice clinical scenarios, real world applications, improve it's going to help you improve retention.
It's like you're soaking yourself in.
It's like you're getting that clinical in that you never really got as a student. What about the other endocrine concept? Hypothalamus to pituitary to target glands. central control of hormones via releasing or inhibiting hormones increased TSH decrease free T4 to you know leads to hypothyroidism usually Ashimoto's autoimmune decrease TSH increased free T4 may be hypothyroidism that's graves disease is common cause of that type 1 diabetes militis autoimmune destruction to absolute insulin deficiency leads to required you know insulin replacement what about type two diab Diabetes is insulin resistance to plus relative insulin deficiency will lead to you managing it with lifestyle and metformin. So type 1 diabetes and autoimmune destruction you know uh type two diabetes is insulin resistance due to weight gain and lifestyle changes.
Now Cushing syndrome is excess cortisol will lead to central obesity, try hypertension, glucose intolerance. You've heard this a lot now, right? It's looking like a repetition now. That is what it should feel like. That is what studying is all about. It's about soaking you all in it.
Listen, there are no strategies without content. Absolutely none. Stop looking for questions. Staff focusing on content. When you have your content, you can answer so many things. Dr. Kinda speaking here, founder and CEO of NP certification academy to reach us nurse to nursecoach atgmail.com or ww.npcertificationacademy.com.
You can also visit us confidentprescriber.com if you pass your boards already and you want to you know just sit in after you pass and you want to sit in and and gain more knowledge. So let's continue here with Addison's disease adrena insufficiency fatigue hyper pigmentation hypotension hyponetriia.
What about primary hyparathyroidism, increased PTH, hypercalcemia, kidney stones, bone pain, SADH, excess ADH, hyponetriia and uolimia plus concentrated urine with diabetes inhibitors ADH deficiency, polyura, dilute urine, hyponetriia, levothyroxin, synthetic C4 for hypothyroidism. Monitor TSH for dose adjustment. Metivas will block thyroid hormone synthesis. You want to avoid in them in the first trimester. Metformid will decrease epatic glucose production.
It is the very first line type two for type two diabetes. With insulin we need it for type 1 diabetes. In cases of type two diabetes when we have resistant to metforming we're going to go to insulin as well. GLP1 agonines will increase insulin secretion. you want to it's going to promote weight loss and cardior protective is also good part of GLP-1.
Now SLGT2 inhibitors that will promote glucose excretion via kidneys. So it is very very good for heart failure patients. Bisphosphonate will inhibit osteoclast to treat osteoporosis risk of jaw osteo necrosis. You got to pay attention to the risk here because when you're giving this med you need to also educate the patient. Let them know what they are getting into. It's only fair. It's only ethical. Hydrocortisone replacement for adrenal insufficiency.
It mimics circadian rhythm. Sabagloin dopamine agonies to treat prolactinomas, shrinks tumors, reduces prolactin levels. That ends our endocrine system.
Speaking as Dr. looking Elisha. You can visit our website for multiple resources and a lot is to come and we look forward to having you in our community of students and community of experts. Do we have any questions at this time? I really hope I didn't bore you. We actually finished earlier than I thought. So, what I'm thinking about doing right now, we skip the questions on lab, right? Can we take some questions on lab now that we have time to actually do it? What do you all think? A 37 year old woman. 37 year old woman keyword present with fatigue.
Fatigue keyword weight gain cold intolerance. Of course you know what it is is already. Well, you suspect hypothyroidism. That's a cheap question right there. They will never tell you that. But at least we know it's hypothyroidism already anyway even before the question said it. Which of the following is the most appropriate initial test? A T3 B uh you know antiPO antibodies C TSH uh D reverse 3. What do we think?
Please drop your answer in the chat. The final answer is going to be TSH. We're talking about whenever we talk about hypo hypothyroidism, your TSH is always one of the first line test to do. So for assessing thyroid function if elevated, you want to confirm with free T4. So free T3 is it fluctuate a lot and it's not the best test and is more helpful with iPadism instead. Anti-TPO antibodies is useful for confirming autoimmune like Hashimoto's but is not for initial screening. Reverse three.
That one is rarely used in routine primary care, but of course sometimes it's used for critical illness to assess T3 clearance. Let's now take the last question here. It's a 53 year old man with central obesity, hypertension, and elevated triglycerides. You are evaluating him for metabolic syndrome and diabetes. So, which lab provides an overview of average of glucose uh levels over the past 3 months? This should be a piece of cake for every provider in the house. Is it random glucose? Is it you know hemoglobin A1C? Is it oral glucose tolerance test? Is it fasting fasting insulin? We know the final answer is hemoglobin A1C. B is the final answer.
Okay. Hemoglobin A1C reflects two to three months average of glucose levels and it's a key test for diagnosis and monitoring. Uh what is incorrect? random blood sugar uh level uh useful for uh in acute settings uh but doesn't reflect chronic uh you know control or glucose tolerance test that one is more cumbersome really it's used for I know I remember doing this when I was pregnant they have to check your health when it comes to whether you have diabetes or not typically used for uh you know when A1C your fasting glucose is borderline now fasting insulin may suggest insulin resistance but not diagnostic for diabetes is B is the final answer. So, please get the rest of the lab questions done is in your slide in Canvas. Uh don't forget stay in Canvas. Don't go from review to review. Too many resources will will not be a good thing.
Don't forget also if you're testing this week or anytime, make sure you don't change your answers at the last minute.
When if you change more than three questions, you're doing too much. Okay?
You got to slow down and walk away from that screen. But if you're changing because you're really sure or because you miss something, then that's okay.
When you flag an a question, it doesn't hurt to if you don't go back to unfl flag it. You can flag your question if it's too thick, but make sure you spend no more than 1 minute on every question.
We are here to support you and we're going to continue to support you. Thank you so much for trusting us and we don't take this lightly at NP Certification Academy. We're now going to move to the next body system. Do we have any questions? Thank you. So when we talk about genital urinary system what are the list of common disorders under the genital urinary system we have UTI benign prostatic hypoplasia nephrolithasis intesticial cyitis epidemitis testicular torsion prostit prostatitis hydronosis polycystic kidney disease urinary incontinence bladder cancer real failure sexually transmitted infections Vzicolor reflux, fmosis, verico cell.
Now these are commonly tested concepts.
Can we know all of this? In general, you have to know 150 diagnosis to pass this exam. I don't have to diagnose will come with how much you soak yourself into the content. So let's quickly go ahead and start with the diagnosis and see how we can remember a lot of this. It's not a very common body system, but you can do it. Dr. Kendasha speaking here, founder of MP Certification Academy. The first thing we're going to be talking about right now is urinary tract infection. So what are the things we're going to see when somebody have UTI, disura, frequency, urgency, supraibic pain and the differential? What is the differential? Meaning what else look like it? It is vaginitis, STI like clamdia and gonora can also look like a UTI. So that means we should be we have to work them up for those things that we suspect and those things that we think are very very close to it. Uh now why differentiate vaginitis lack bacteria?
That is how you're going to nail your question on the exam. Vagitis they lack bacteria.
STI often have discharge and systemic signs. What about labs and diagnostics?
urinalysis like polyura, bacteria, urine culture are the things that we do. The very first line treatment generally is antibiotics like nitrofertoine you know sulfur drugs are the first things that we do. Now UTI though can take another form and shape in a geriatric. Let's keep that in mind. we may need to go ahead and you know sus we going to we need to make sure when our when they are like having confusion we're going to rule them out for all that cognitive confusion at the same time we work them up for UTI but whenever we see confusion our geriatric population is most likely UTI related.
Now what about benign prostatic hypoplasia, urinary escotancy, weak stream, nocuria, the key symptoms, uh prostate cancer, prostatitis are the things that kind of overlap or that look like it. Cancer has nodules, elevated PSA, prostatitis has fever and pain. So digital rectile exam, PSA, ultrasound of if needed, these are the are the tests that we do. Alpha blockers, tams tulosin, uh five alpha blocker reductase inhibitors, uh finest are the things that we can use to support this patient.
Now nephrolithasis uh like kidney stones is another name for nephrolithiasis.
Severe flank pain think about where this is from and connects the dot. Nephro kidney is more on the flank area.
Immaturia, nausea are the things we're going to see. Now, uh, pyon nephritis, muscularkeeletal pain are the things that overlap the differential diagnose that overlap nephrolythsis.
So, what are the signs though? Um, in general, uh, pyon has fever, systemic um, symptoms, muscularkeelet.
So, pylon has fever, systemic symptoms, excuse me, sorry about that. Uranis uh, immateria um is what we're going to be looking for when we do an analysis. We can do non-contra CT abdomen or pelvis to rule out nephrolithis.
Now when somebody have kidney stones, I'm I'm sure you've heard about it. Pain is crazy. So pain, we're going to do some NSAIDs, hydration, uh possible uh lithotripsy. Now what about intesticial cyitis, pelvic pain, urinary urgency or frequency, nocuria? Now UTI, bladder cancer are the things that also look like intestial cyitis. We must understand what the differential diagnosis is. So UTI has passive urine culture. Cancer often has immaterial mass. So that is how you're going to separate it. What separate them then?
UTI has passive urine culture. Cancer is often with immaturia and then we also see the mass that comes with it.
So what test do you want to run then?
Cytoscopy analysis.
And of course we would see if it is uh interstitial societies supposed to a lot of times we say like negative culture lifestyle changes blunder blunder installations and of course uh p uh ptocin uh polyulfate are the things uh that we can use as a very first line treatment. So what are we paying attention to the case symptoms the common differentials like why why are they different and then what labs are we going to use to finally nail the original diagnosis and what is the first line for taking care of it the next thing is going to be uh epidma epidemiitis that is a scrotal pain or swelling that is the definition that's the part that's not a part that's just a definition that's what we see patient comes in with scrotal pain swelling fever dysura that would that would kind of connect you with what epidmite is.
And what else can also look and sound like this though? Testicular torsion can sound like this. You know, okitis can sound like this. And that makes it a differential diagnosis. Differential is what else look like it? You know, torsion is sudden onset with absent cremosic reflex. Oritis involves what?
Testies. And then we have urinalysis crual ultrasound um as the test that we run. How do we treat antibiotics like doxycyc and septrianzone if STI is suspected? What about testicular torsion? Sudden testicular pain, swelling uh is what we see with testicular torsion. Just think of torsion as twisting. Something is twisting. You know it's serious. If it's twisting, it's also cutting off blood supply right now. And so sudden severe testicular pain and swelling, epidemitis, torsion of the appendix are the things that look like this diagnosis. But how is torsion different though? Tossion has a absence what creastthetic reflex that is what makes it that's what sets it apart and it's very rapid in onsense. Uh then what are we going to do to rule it out? Scrot ultrasound decreased blood flow is what we're going to see on that ultrasound.
And then surgical urgency you know detrion we have to make sure we untwist it and oiplexi plexi oixy.
What about proatitis is a what do we see? We see pelvic pain disura fever malaise. What exactly look like this? What else we can be described this way? It is BPH benign prostatic hypoplasia or UTI. But benign prostaticia usually is chronic. Then there's no fever. So they're not like sick the whole time with fever all over the place, right? UTI will lack pelvic pain and it also has fever with it.
Urinolysis, prostate secretion, culture, and these are the things that we do to rule it out. Antibiotics like fluoconolones are things we're going to get. Yeah, that is a big guy right there. But we need something strong like that to tackle and deal with the bacteria that led to this prostatitis before it leads to something else.
Hydronnephosis. What do we see with hydrononephosis? We see flank pain, nausea, urinary difficulties, nephrolletthasis, uh pyo pyon nephros, nephritis are the things that look like hydro nephrosis. But what are the things um that set them apart? So stones can cause acute pain generally necrosis and of course pyon nephro nephis has fever that is what set it apart. Okay. So what do we do to rule this condition out?
Ultrasound. In ultrasound, when we take it, when we do it, what do we see? We're going to see dilated renal pelvis, you know, relieve obstruction, and then we're going to have to treat the cause.
Polycystic kidney disease, PKD. We see flank pain, immaturia, hypertension, abdominal mass, renal cyst from other causes is also a possibility. family history, cyst distribution on imaging, ultrasound or CT scan are the ways to rule this out. You want to control blood pressure for this patient with ACE inhibitors and you want to do other kind of supportive care. Okay, urinary incontinence that one is just licking urine uh you know urgency nocura that are this definition of incontinence and of course UTI will be on your exam is going to dance around it. So we have all kind of incontinence and we're going to be talking about that at some point.
Then UTI overflow uh incontinence pelvic prolapse are the things that also look like urinary incontinence. So UTI has infection signs with it overflow due to obstruction is what we see with the overflow incontinence. So analysis postvoid residual volume behavioral therapy anticolinergic uh checks are things we can do to help with the urge or depending on the type of the UTI incontinence that we have now bladder cancer is painless immateria painless it's cancer but it's painless but you're seeing blood in your pe and you're peeing frequently UTI nephrolithasis are the things that look like bladder cancer UTI will show infection stones and cause pain. Urinolysis, cystoscopy, urine cytologology uh are the things that we can run to rule this this patient out. Trans urethra or uh resection, chemo or radiation are the ways to resolve this issue or to minimize its progression. I don't think there's a permanent resolution but we can slow down its progression. Renal failure. Renal failure. What are the symptoms that we see with renal failure? We see fatigue, edema, decrease urine output, fatigue, edema, decrease urine output. It only makes sense. It's a renal failure. What else look like it? We cannot think, oh, maybe the patient is dehydrated, maybe they have a heart failure. Those are the differential diagnosis that things also look like. So, how do we distinguish with lab? Then we're going to just check out the courses and make sure we work them up. We have to do like bun, creatin, electrolytes, you know what I mean? To see what exactly it is. renals you know our B and creatine will tell us if it's a kidney problem or not you want to treat the underlying cause if it's so bad diialysis may be the next option STI example chlamydia gorrhea duria discharge and pelvic pain are the things that we see with STI you will see dysura you will see discharge you will see pelvic pain pain UTI vagitis are the comorbid conditions that goes on with STI STI often has discharge, sexual history, then we need to do the NAT test, NAT test, urine culture to rule out STI, antibiotics like doxycycling. Again, this is not set on stone. We have to look at what population we're dealing with to make a conclusion on our treatment choice or treatment of choice.
You know, are we dealing with pregnant mom? Is it pediatrics? Is it geriatrics?
Is it adolesccent? Do they have HIV? Do they have renal problem? So we have a lot of things to think about before we make a choice. Are we going to go with monotherapy if monop therapy is not working? Are we going to be adding a lot of drugs together to make a combo that works for them? So anyway for now when we talk about treating STI but choosing doxycyc or sept triazone what about vicorate renal reflux recurrent UTI we see flack pain and that's what we see vesicle red reflux.
What else look like this condition? UTI, pyon nephritis and of course what labs do we need?
Um definitely reflux is diagnosed by voiding. Um generally the void and um we also do ultrasound you know ultrasound actually I think is the place preferred for this kind of a thing physical phys because you want to be able to pick up where and sometimes they they step it up to a bigger scan as well antibiotic you know prophylaxis surgery if it is needed fimosis just a tight foreskin painful urination I'm sure many of us if you work ICU med surge you've dealt with femosis maybe not the condition itself but a lot of times patients are not probably circumcised when they have this condition too so they have this tight for skin the condition that goes with it is balan balanites paraphimosis you know now balanitis has inflammation is the difference from balanites and paraphimosis Balance has inflammation. Paraphimosis is definitely an emergency. Femosis itself is a tight fork skin painful urination for the most part. When we do clinical exam, we have to just um decide how you know which one it is or what to really nail the diagnosis on. How do we fix this? Generally though, we're going to do topical steroids, circumcision of course if needed. I don't even know the age limit of for circumcision. I'll be I'll be curious to look into that as some for next time. But when we see this condition, they just are not circumcised.
Now varico cell scrotal heaviness infertility hydro cell testicular tumor are the things that also look like varico cell but if you have to separate those things hydroel is painless painless swelling and then of course the tumor is just a tumor. It's got a mass with it. So hydro cell you know is painless.
So we have scrota ultrasound okay that we have to do to rule this condition out of varico cell and then observation surgery if symptomatic.
So now special population here this is now where things becomes a little bit isolated. This is extra noise that we must have when they put a pregnant woman a child on your exam. Those are key words that you have to pay attention to.
If a pregnant woman have a UTI for example, we're going to see the same symptom though. Duria, frequency, urgency, fever and so on and so forth.
But how do we treat it in pregnant in a pregnant patient? We're doing nitroferent in all separine. But you want to avoid sulfur during the first trimester. extremely important to please focus on your treatment to the right side of my slide for your special population right there. You want to monitor right now uh children weight-based uh antibiotics can also be you know used as a treatment. Now what about BPH?
You know older men more than 65 years old, they have urinary retention, they have wigstream, you know prostate cancer, we need to screen them for that with PSA. It's not required uh to do this um you know how you do this prostate exam because it's not really specific. There's a lot of controversy controversial stories about that. So alpha blockers tamillosin you want to monitor for autostatic hypotension you know you want to monitor for autostatic hypotension when you're giving BPH because it's an alpha blocker but that is the main state treatment for BPH benign prostatic hypoplasia now nephrolithis children or elderly you want to make sure you manage the pain pain control mean children be careful with NSA dosing what about Intesticial cyitis you want to do bladder training uh pentosan poly sulfate avoid irritants like caffeine and alcohol epides less than 35 you want to treat STI doxy plus the septriazone more than 35 you want to do fluoroquinolone this is also age specific okay fluorocinone like leopassin for someone that is more than 35 sept triazo for someone that is less than 35 if they have epid epidis.
Okay. What about testicular torsion?
It's an emergency. You want to want to pre the torsion means untwist it and of course octopi are the two options that we can do for testicular torsion. Now prostitis antibiotics tailored to acute or chronic fluorocinolone is very common. What about hydro nephrosis? Relieve obstruction, treat underlying cause. You want to monitor fetus. What about PKD? Blood pressure control, renal protective agents and diialysis if needed.
We're now going to go on to urinary incontinence. Behavioral therapy, pelvic floor exercises are the things we can do as well as antiolinerics.
For bladder cancer, trans urethra resection, intravestical therapy are the things that we can do for renal failure.
Treat underlying cause dialysis if needed for STI. Antibiotics pathogen partner treatment. Vesic corrector antibiotic prophylaxis surgical correction if severe. Femosis topical steroid circumcision if recurrent or infection. Varicosel observation surgery if symptomatic or infertility.
So that ends our question, our content on genitalary system right there. I hope you learned something. You now have to repeat and repeat and repeat this slide.
You will be getting to access my audio.
You also repeat and repeat and repeat this audio.
Now we're going to go into questions now. However, I see the answers are right there, but we're going to see if we can make it a simulation quickly.
I know we are past time. If you have to go now, it's okay. But let's quickly wrap up here. A 28-year-old sexually active woman present with dysura, urinary frequency, and supraubic pain.
Her urine dipstick is positive for nitrate and luccoytes x-rays. She denies vaginal discharge. What is the most likely diagnosis? A vaginitis. B urinary tract infection. C pelvic inflammatory disease. D intesticial cycitis. So key words that you want to also pay attention to on exam is is bold here.
Disura durary frequency suprapubic pain.
Automatically we know that this one is going to be UTI. The presence of dysura frequency suprapubic pain. These are positive nitrate and positive nitrates as well as luccoytes. It is UTI. Vagitis typically present with what?
discharge and vaginal itching. P as lower abdominal pain, fever, cervical motion tenderness. Interest usually as negative urine cultures. Let's look at question number two. The 65 year old is a keyword. Man completes of difficulty initiating urination, weak urinary stream and nocura. On digital rectile exam, the prostate um is enlarged with smooth uh but smooth PSA is mildly elevated. What is the most likely diagnosis? A prostate cancer, B benign prostatic hypoplasia. C prostatitis, D bladder cancer.
Of course, key words here again says what? Difficulty initiating urination.
And this is a man and is 65 years old.
more than 65 they have a chance of getting enlarged prostate. So we know and then the stream is also slim and of course they can they also having noia because every time they continue to feel like something is in their bladder PSA is mildly elevated there is no doubt here this is straightforward this is benign prostatic hypoplasia. So what is BPH? It present with urinary hesitancy with extreme nouria or in older men. Uh prostate cancer often present with nodules and or asymmetric enlargement and significantly elevated PSA.
Prostitis often has fever and perennial perennial pain bladder cancer present with painless immaturia.
Now the next one here is question number three. It's a 16 year old male that presents with sudden onset sudden onset of severe left testicular pain and swelling.
The creastthetic reflex is absent on the affected side. What should be the immediate next best first step? A start antibiotics and observe. B order scro ultrasound and schedule surgery if needed. C immediate surgical exploration for testicular ation. D prescribe pain medication and follow up in 24 hours.
How careless is that? Right. Some answers are right off the bat wrong. You will be able to know what to to knock out of the way. Two answers are obviously generally wrong on the test and two will be close. The final answer is going to be C. So immediate surgical exploration for testicular torsion.
Sudden severe testicular pain with absent crema reflex is a classic sign for testicular torsion. A surgical emergency needing immediate detortion to save testicle delay can result in testicular necrosis.
Question number four. 45year-old woman has chronic pelvic pain, urinary urgency and frequency. You see how similar these things are? So you're going to sit down and make sure you study with study this slide. See the pattern. See how to differentiate this all of this. But negative urine culture. But when they give a butt on your question, they have they've given you a little detour, right? But negative urine cultures and no signs of infection. Which diagnosis best fits uh is fits best? A recurrent UTI, B intersticial cicitis, C bladder cancer, D ur urethritis. So we know this is going to be intesticial cyitis based on the key symptoms of what pelvic pain urinary urgency and frequency and of course negative cultures meaning it is going to be intestial societitis and of course we're going to rule out infection because of malignancy because there is no mass there is no infection there's no fever right so now B uh is the final answer institial cyitis question number five a 5-year-old girl present with recurrent urinary tract infection.
They've had urinary infection but it keeps coming back and they keep having they're having flank pain with it.
Imagine shows abnormal urine flow from bladder back to urittors. What is the most likely diagnosis? A vesicular rectile reflux B nephrolithis C hydrononephosis. D pyon nephro nephritis. We know the final answer is what? Viculcta reflux. And that is because the recurrent UTI that we are having and and of course it keeps coming back and now we're having flank pain with it. Uh you know what I mean the urine point to flow vicular rectal reflux then they're common in children and of course that they have a risk of pyon nephritis eventually when it graduates. So it's something worth paying attention to. So vicul reflux is going to be the final answer for that.
Question number six is a 55 year old man that completes of left flack pain, immaturia and nausea. He has a history of dehydration and recently had episode of intense exercise. Your analysis shows microscopic immaterial but no infection.
What is the most likely diagnosis? A pyon nephritis. B nephrolythosis. C bladder cancer. D acute tubular necrosis. This is a complaints of left flank pain. Immaturia and nausea. Left flank pain. Immaturia and nausea. What do we think? We know the final answer.
It's going to be nephrolithiasis.
Flank pain, immaturia, nausea, but no infection suggest kidney stones.
Nephroliththiasis.
Pyonas generally will present with fever and positive urine cultures. Bladder cancer usually present with painless immatur. You see how they are different.
Now acute tubular necrosis will relates to kidney injury not acute symptoms.
Let's look at question number seven. So 70 year old woman that report involuntary leakage of urine when coughing or sneezing. She has no fever or disura.
The condition is most consistent. Which condition is most consistent with our symptoms? A stress urinary incontinence.
B urinary tract infection. C overflow incontinence D interstial cyitis. Let's take a look. It says involuntary leakage but when coughing that makes it some kind of incontinence right there. That should be your clue. So automatically you ring out B you're taking out D and then you're going to hold on to A and C because it says stress incontinence or overflow incontinent and you know this is some kind of incontinence. By definition stress incontinence comes with coughing, coughing or sneezing excuse me. So that is a final answer.
Stress incontinence overflow is dribbling due to some kind of like blockage. Does it make sense? And they provide this weak strain. We don't have that here. Okay. Let's look at question number eight. A 30-year-old uh sexually active male that present with crotal pain, swelling, and fever. I am letting you This is like a skills class. We're not really throwing multiple pictures in, but we're trying to see what differences we can see with all of this counselor because they run together for most students. Ultrasound shows what blood flow in the epidmite.
What is the best initial treatment? A surgical exploration. B. Antibiotics targeting STI. C. NSAIDs and watch for waiting. D urinary cathization.
We know the answer is going to be antibiotics targeting STI. Why is that?
Symptoms suggest epidemitis. That's the that's the first thing you want to do.
What is your diagnosis? Yes. Coral swelling, fever and swelling. I mean scalo pain, fever and swelling. That is epidemitis and it's often due to STI especially in young men. It increase blood increased blood flow in on the ultrasound support inflammation.
Treatment requires targeted antibiotics like doxy and septrias.
Question number nine. A pregnant woman in her second trimester. Now we mentioned a pregnant woman. Let's pay attention to that population especially comes in with dysura urinary incontinent frequency but no fever urinary urine culture grows more than 100,000,000 cfu per ml. Okay. What is the appropriate management? A no treatment needed. It's a symptomatic bacteria. B oral antibiotic safe in pregnancy. C hospital admission for IV antibiotics. D start antifungal therapy. Oralo antibiotics safe in pregnancy. Um uh what is that? Because this is an asytomatic antibacteria in pregnancy bacteria in pregnancy and we need to treat it to prevent pylonritis. Now pyonitritis is a big one. We don't want things to get there. Okay.
Nitrofarentoine or sephylexine is great and they are commonly used.
Nitroferentine is compatible with our pregnant moms. They ask you for the first line for anything that has to do with the kidney. Nitrofarentine and you will not be wrong. We don't hospitalization is reserved for pyo. We don't put everybody in a hospital otherwise we're not going to have space.
Right. Question number 10. A 40 year old man present with painless immaturia and increased urinary frequency. Painless immaturia and increase urinary frequency. Irunalis is positive for blood but negative for infection. What is the next best step in the management?
A start antibiotics. B order cystoscopy.
C prescribe N6. D reassure and observe.
And we know the final answer is going to be to order a cystoscopy. It makes sense. We are suspecting bladder bladder cancer here. Bladder cancer is what we're suspecting here. Or other malignancies. Cystoscopy is required for diagnosis. Antibiotics are inappropriate without infection. Let's look at question number 11. A 23 year old woman presents with dysura increased urinary frequency uh cloudy urine. She reports recent unprotected sexual intercourse and of course urine dipstick shows luccoytes estrays positive but nitrates are negative. What is the most appropriate next step? A start empiric antibiotics for UTI. B test for STI such as clamdia and gonora. C advise increase fluid intake only. D order renal ultrasound. So here we're talking about patient with dysura is a key word.
Increase urinary frequency is a key word. And then cloudy urine. Okay.
automatically you know there's some kind of STI going on here and then we have to test for STI for sure like clamia or gonora in sexually active young women the serialia frequency and cloudy urine definitely we are looking into STI STI are important differential empiric antibiotics like for STI may miss the underlying STI so we don't want to do empiric want to assess first all right now question number 12 is a 60 year old male complains of grad Gradual onset of urinary hesitancy. Gradual onset of urinary esotancy. Right. Noia and weak stream. PSAs within normal limit. DR reviews enlarged but smooth prostate.
What is the most likely diagnosis and appropriate force line treatment? A.
Prostate cancer. Prostatectomy. B. Pph alpha blockers. C. Prostat prostitis antibiotics. D. bladder outlet obstruction cathization. We know define as BPH, alpha blockers. So typical urinary existency and nocturia with enlarged smooth prostate um and normal PSA is consistent with BBH. Alpha blockers, relaxed prostates, smooth muscle as the first line treatment.
Question number 13. A 12-year-old boy present with sudden onset of severe scrotal pain and swelling. The cremaic reflex is present. The Doppler ultrasound shows increased blood flow and of course uh to the testes. What is the most likely diagnosis here? This is also straightforward. Is he a testicular bidis?
C hydroil d varicoil. This concept will require a lot of your repetition because I know it's a lot to keep in. Don't forget we have to know 150 diagnosis minimum to pass this exam. You can do it. Epidmitis presence of creastthetic reflex and increased blood flow favors epidmmitis over torsion right with torsion it is treated there's no increased blood blood flow right and there is no cremastthetic reflex with torsion which typically has absent and decreased blood flow all right so that is pretty much it I only have a couple of questions left go through the rest of the questions and um we can just do this one asked when a 35 year old pregnant woman because of special population and uh at 28 weeks gestation report this ura and urinary frequency urine analysis shows lucco sites but no nitrates and urine culture is pending which antibiotics are the safest for empiric treatment nitrintoine avoided near-term or or sephyllexin b fluorocinolone c trimeropazol d tetrayline and we know the final size nitroen. This is the deal.
This will look like a lot. Okay, you this is the way to do it. If it's your first day, if it's your first week, your second week or third week, take a look at where am I really at? Do I really know this stuff? Are they foreign to me?
Whatever I don't know, let me check it out. That is where you're going to expand your library. When you're studying for advanced practice register registered exam, you are have to expand your library because there's a lot of concept and content to pick up on. labs to worry about, special population to worry about, first line, second line to worry about, FDA approved to worry about and and all kind of guidelines. So, it's a lot. But here we try to put it together by creating your foundation. If you feel no if you don't feel connected with this, I have a pathophysiology content is almost 5 hours. I recorded it. You don't have to do my path, but you must solidify your path.
If you feel disconnected in class today, you need to step away from class tomorrow and just go do your ple. I have the audio in canvas or in our learning platform and go get it there and make sure that you do it. When you solidify your path though for over the weekend or any maybe like for 10 10 to 20 hours straight honestly you will see that a lot of this concept is not going to be foreign. We also have antibiotic foundation that you need to also do that is also recorded. Cerology foundation I have it imunology is also there as a foundation. Pharmacology is there as a foundation. Inducers and inhibitors is there. Drug drug interaction is there as a foundation. So I have a lot of foundation that you have to do. My foundation alone will take you at least 20 to 40 hours in a way. I don't know you're going to find a way to spread it out to be maybe less by repeating and repeating. Just pop it in your ears. If you don't know where it is, check under assignment or check under announcement is also is always going to be there. We also always post on WhatsApp. Uh so always check also check it there. Now again you don't have to do my path but you have to have your path to do this exam even if you don't do other foundations you must have your path but you can do it we believe in you please don't give up on yourself Elisha speaking here founder of MP certification academy to reach us nursecoachgmail.com um or email um [email protected] you can also call us up 3479160 6037.
Do we have any questions at this time?
We are now done completely. Thank you so much for sticking it out with me today.
We are now done with the endocrine system. We are done with the gentleary system. We do some questions in between.
We put in some critical thinking application and also don't forget you have to have your content. You have to know how to diagnose. Your diagnosis will come but it's not going to be overnight. But you can do it. Our structure here at the academy is simplification, repetition and retention. As you can see how large the content is. Sometimes you come in, we also moderate our audio. So you can be guaranteed to do well on your exam. Um because you are connected with somebody at some, you know, at some point like whenever you come to class, you're connected with a real human being. Uh so we look forward to seeing you succeed.
Thank you so much and have a wonderful day.
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