Cram The Pance - S1E30 50 High Yield Endocrine Questions

Episode Date: July 16, 2021

50 high yield Endocrine questions to help you prepare for your Pance, Panre and Eor’s.  ►Paypal Donation Link: https://bit.ly/3dxmTql (Thank you!)--- Support this podcast: https://anchor.fm/scott--shapiro/supportBecome a supporter of this podcast: https://www.spreaker.com/podcast/cram-the-pance--5520744/support.

All right, so let's do 50 high yield endocrine questions. Everybody, thank you so much for the comments, the new subscriptions, everything. I really appreciate the support. And if you haven't checked out the YouTube page, please do cram the pants on YouTube. Okay, so let's go ahead and get started. Question one, patient presents to the office with polyurea and polydipsia. He has a family history of diabetes, and he wants to be tested to see if he is diabetic. He lasts eight two hours ago, and his blood glucose in the office was 156.

Say, once he comes back and reveals a result of 6.3, And his two-hour glucose tolerance test revealed a blood glucose of 212, which one of these labs can definitively make the diagnosis of diabetes in this patient. So the one lab test he had would be the two-hour glucose tolerance test with a blood glucose of 212. Let's go over the results that did not make the cut. So his blood glucose in the office was 156. That was not fasting, though, so that couldn't diagnose with the 126 or higher, which is one

of the factors that we can use to diagnose. has A1C came back 6.3, but we need a 6.5 to diagnose diabetes. And then the glucose tolerance test, which after you give 75 grams of glucose, two hours later, if they're 200 or higher, can make a positive diagnosis. And this patient happen to be 212. So that's what makes the diagnosis of diabetes. The only one we didn't mention would be the random plasma glucose of 200 or higher in the presence of classic diabetes symptoms or complications, like polyurea, polydipsia.

Question number two. Six-year-old male presents to the office today, because his diabetes is out of control lately, and he would like some help getting his blood sugars back to normal. He only currently takes metformin of 1,000 milligrams BID. You discuss a few different medications with him, including glyphezyde, insulin, glargine, and amyglofosen. He states his only fear with starting new medication is low blood sugars.

Which one of these medications discussed with the patient is least likely to cause hypoglycemia? So the only one discussed that would be not likely to cause hypoglycemia would be emphyglofen. The other two, glargine, which is a bit of glyclycemia, which is a basal insulin. As we know, all types of insulin have the potential to cause hypoglycemia. And then glyphezyde, which is sulfonuria. It's an insulin secretagogue, which is notorious for causing low blood sugars. Glypid, gliparide, all the sulfonurias can cause low blood sugar. So the only one, the ampaglofen, which is an SGL2 inhibitor, does not usually cause low blood sugar. So that will be the choice for this patient.

Question three, what is the most common type of thyroid cancer? Most common type of thyroid cancer? That would be papillary thyroid carcinoma, about eight out of 10 cases is papillary thyroid carcinoma. Question four, a non-pregnant adult with subclinical hypothyroidism should be treated with thyroid hormone replacement like lebo-thiroxine when their TSA reaches what level. That would be a TSAH of 10 or higher. So 10 or higher, virtually all sources agree upon treating once this patient's reach to this level to prevent cardiovascular complications, anything less than that, like 4.5 to 10. different sources are going to have different opinions whether or not to treat. It's kind of controversial, but 10 or higher, TSA and subclinical hypothyroidididididism, almost all sources agree treat at that level with libo-thoroxine or another thyroid hormone replacement.

Question five, 27-year-old female with history of bipolar disorder presents to the office complaining of fatigue, constipation, and weight gain. Labs are ordered, and it is determined she is biochemically hypothyroid. What medication is this patient likely taking that led to her diagnosis of hypothyroid? So the medication she's likely taking would be lithium. So the history of bipolar we saw in the vignette, that's a first line medication for bipolar is lithium. So you just have to know that lithium can absolutely cause hypothyroidism. It's a board favor to ask about that. So when you're on lithium, you actually have to have your TSA checked about every six to 12 months because hypothyroidism is so prevalent with this man.

The other one, the other popular men to ask is probably going to be amyodorone. That's another one that can cause hypothyroidism. So anytime you see bipolar mention, remember lithium, and lithium can cause hypothyroidism. Question six, 37-year-old female presents to the office complaining that she is having trouble losing weight, despite following a strict diet and exercising daily. On physical exam, you note central obesity, thin extremities, oily skin, and stri-a across her abdomen. A screening test to check for excess of what hormone should be checked in this patient. So that would be serum cortisol. This patient has pretty classic findings of Cushing Syndrome, weight gain, stri-a, which is.

those stretch marks on the abdomen, oily skin, thin extremities, central obesity. The only thing that's missing from the vignette, because I didn't want to make it too obvious, is a buffalo hump. And with cushings, we know we're looking for increased cortisol levels. Once we establish the increase in cortisol, then we can use differentiating tests to see if it's cushioning disease or an ectopic ACT-H-producing source. Question seven, patient with secondary hypothyroidism will have an abnormality in which part of the hypothalamic pituitary thyroid access.

So secondary hypothyroidism, that is going to be. be the pituitary gland. So secondary hypothyroidism is that caused by a TSAH deficiency. As we know, the pituitary gland is responsible for TSA production. So anything like a pituitary tumor, Sheehan syndrome, which is that postpartum pituitary necrosis, they can all be responsible for secondary hypothyroid disorders. Question eight, what is the most common cause overall for Cushing syndrome? Most common cause overall for Cushing syndrome, that's going to be long-term high-dose use of glucocorticoids. Question nine.

And a patient with diabetic ketoacidosis, DCA, after checking capillary glucose levels and confirming urine ketones, to confirm the diagnosis, was the first therapeutic intervention that should be started in these patients. So you've confirmed DQA, what's the first thing you're going to do to treat them? That's going to be start IV fluids. So the first crucial step in treatment of DQA is infusion of isotonic salines. Patients are severely dehydrated. After that, or at the same time, you can start to replete potassium. give insulin, but right away, these patients need IV fluids. Question 10, a 69-year-old female with type 2 diabetes for over 25 years, presents to the office today complaining of early satiety,

epigastric discomfort, and post-prendial nausea, and bloating for many months. What is the likely diagnosis in this patient? So in this patient, the likely diagnosis is going to be something known as diabetic gastroporesis. So diabetes is the most frequently recognized disease associated with gastroporesis. And gastropreasis is a lot of gastropresis. And gastroprecy is a lot of is it's just a delayed gas for emptying and it's caused from years of damage from diabetes. It leads to autonomic neuropathy, which affects the vagal nerve and just basically reduces the frequency of contractions of the stomach, of antral contractions leading to this slowed emptying of the stomach we see in diabetic patients.

Question 11, a patient with nephrogenic diabetes insipitous will likely have what response in urine output after a desmopressin ADHD stimulation test is performed. So a patient with nephrogenic diabetes insipidus, you give them desmopressin, which is artificial ADHD. What's going to happen to their urine output? Nothing. There's going to be no change. You're going to have continued production of large amounts of dilute urine because this patient

has nephrogenic diabetes insipidus. So there's no problem with ADHD. It's the kidneys are just ignoring it. They're insensitive to ADHD. You compare that to central, which is a lack of ADHD production. You give somebody with central diabetes insipidus ADH, desmopressin. They're going to have a reduction in urinary output. They're going to improve.

So I used to remember diabetes insipidus, the DIA in diabetes insipidus. In central, the DIA stands for a decrease in ADHD. And in an ephrogenic, the DIA and diabetes insipidus stands for decrease in acknowledgement because the kidneys aren't acknowledging the ADHD. Question 12, what medication class if given to a patient with feal chromocytoma, before initiating treatment with alpha adrenergic blockers like phenoxybenamine can cause unopposed alpha constriction and lead to a hypertensive crisis? So what med before giving alpha blockers can lead to this hypertensive crisis in a feochromosytoma patient?

It's going to be beta blockers. So after you've initiated treatment with your alpha blockers and you've achieved adequate alpha adrenergic blockade, then you can start your beta blockers like propranolol, matoporilol. This is normally done preoperatively, but you never start beta blockers before alpha blockers. You can cause hypertensive crisis in a patient with a feocromositoma. Question 13, what is the most common cause of hypothyroidism in the U.S.? So that is going to be Hashimoto thyroiditis. It's a chronic autoimmune hypothyroidism, and it's the most common cause in the U.S.

of primary hypothyroidism and other parts of the world that they call iodine-sufficient areas of the world. So the U.S., obviously, we don't typically have iodine deficiency. Other parts of the world that do, that's going to be your most common cause of hypothyroidism. But here in the U.S., it's going to be Hashimoto thyroiditis. Question 14, a patient with history of Graves disease presents with bilateral, scaly non-pitting in duration of the skin of the lower extremities with brown patches spread throughout what is the name of the likely diagnosis in this patient so that's going to be something known as pre-tibial mix edema it's an autoimmune reaction that can be seen in patients with graves

disease and it's caused from this excess or this accumulation of something known as glycosumino glycans which collects in the dermis of the skin can cause these swollen rat like red or brown patches and this non-pitting edema which is key because that different It differentiates it from other causes of lower leg edema like CHF, which has pitting edema. So this is non-pitting. That's kind of the key to the vignette there. Question 15. When treating a patient with Graves disease, which medication should be used in the first trimester?

So pregnant patient Graves disease, what matter are you going to use in the first trimester? That's going to be your PTO, your propyl thyracililil. So you use PTO in the first trimester. And then you can start on methamazole after that. So PTO in the first trimester, then you can switch to methamazole. And really, PTO in the first trimester is really the only time you use PTO over methamazole. Methymazole is generally preferred. But first trimester, you can't use methamazole.

The way that I used to remember that, PTO stands for pregnancy trimester, uno. That's how you remember you use PtU in the first trimester. Then you can switch over to methamazole. Some guidelines say you can use PTO the whole time if you wanted to, but most guidelines are you going to say P2 first trimester, methamazole for the rest. Question 16, a patient develops bladder cancer and is suspected that one of the medications he uses for diabetes is to blame. which diabetes medication is this patient likely taking. So the medicine is likely taking that led to bladder cancer would be P.O. Glittosone.

Stroke carries an increased risk for bladder cancer. It's in the TZD class along with rosyglytosone. The way that I used to remember, Poglidicone is associated with bladder cancer, as I just sort of remember P. Oglitosone. So you think of peeing and then you think of the bladder. Remember, it's associated with bladder cancer. Question 17, a patient with Cushing's disease, which is a pituitary cause. After administration of high-dosexamethosone,

will likely have what response in their serum cortisol levels. So that would be a suppression of serum cortisol. So Cushing's disease, a pituitary source, is the only type that will suppress with high-dose dexamethosone. All the other ectopic sources of Cushing's syndrome like adrenal tumor, atopic-T-H-producing tumor, steroids, they're not going to suppress in that high-dose dexamethosone. It's only your Cushing's disease, your pituitary source that will. Question 18, a 47-year-old female presents to the all. office two weeks post-stop after having a thyroidctomy performed. She complains of muscle cramping,

muscle spasms, as well as a tingling sensation in her extremities. An ECG is performed and prolongation of the QT interval is visualized. What is the likely cause of her symptoms? So likely cause of her symptoms is going to be hypocalcemia. So she has an iatrogenic cause of hypoparithyridism. And we see this in patients who recently had a thyroidectomy performed. It can cause about 3% of hypoparothyroidism after a thyroidectomy. So during the surgery, whether they by accident cut out some of the parathyroid glands, there was a thermal injury from the cauterization to the parathyroid glands, whatever the case, they destroyed or remove the glands, and it led to hypoparithyridism with result in hypokalcemia, which the patient has a classic presentation, paristhes, muscle weakness,

and then most importantly, that prolongation of QT interval on ECG. Question 19, a 37-year-old female presents to the office today because she has not had her period in four months. She is not sexually active and denies any chance of pregnancy. She also complains of headaches and a milky discharge from her breast. What is the first line medication class for the likely diagnosis? So that would be dopamine agonis like haveragolin, bromocryptine. So the patient in this vignette with aminorrhea, galactoria, headaches, which is caused from a compression from the adenoma, likely has a prolactinoma. It's the most common type of pituitary adenoma. And the reason we use dopamine agonis, well, the primary function of dopamine is to inhibit prolactin. So dopamine

agonists, which mimic the action of dopamine, are going to decrease prolactin secretion and synthesis. Question 20, multiple endocrine neoplasia type 1 is a rare autosomal dominant disorder characterized by predisposition to tumors most commonly in what three areas of the body. So that is going to be your three P's, parathyroid, pancreas, and pituitary. The clinical spectrums kind of expanded. Some sources include the duodenum adrenal, but most commonly, the one you need to know for the boards is going to be your 3Ps, your parathyroid, pancreas, and pituitary for multiple endocrine neoplasia type 1. Question 21, a 56-year-old male with history of diabetes presents to the office today to review recent lab results. His labs show he is deficient in vitamin

B-12, which medication is he likely taking for his diabetes that caused a deficiency in vitamin B-12. So that is going to be metformin. Metformin can reduce intestinal absorption of vitamin B12 and cause deficiency, vitamin B12 deficiency in about 5 to 10% of patients taking the medication. Question 22, what is the most aggressive type of thyroid cancer? By far, that's going to be anaplastic thyroid carcinoma. So it's extremely aggressive, which is actually quite different from the other types of thyroid cancers. And the median survival time from diagnosis is in the range from about three to seven months. Question 23. How soon after the initiation of thyroid hormone replacement, like with lebothyroxine, and a patient with primary hypothyroidism, should the Tsh be checked?

So that is going to be four to six weeks, four to six weeks after you start lebothyroxine or whatever thyroid hormone you're using, armor thyroid, etc. You check the TSA to see if you're giving enough or too much, and then you can make the adjustments from there. So four to six weeks after initiation. Question 24. 42-year-old male presents today to the office for routine labs. The results of the labs show an elevated T-SH level and free T-4 levels, which are within normal limits. So elevated T-SH, normal free T-4. Patient is otherwise healthy and asymptomatic.

What diagnosis should be suspected in this patient? So you should be suspecting subclinical hypothyroidism. So isolated, increased T-SH with normal serum-free-T-4 in the absence of any symptoms or clinical manifestations of hypothyroid. You should be thinking subclinical hypothyroidism. So remember that isolated increased TSA, really no symptoms for the most part. Sometimes it can have these mild, vague, non-specific symptoms. Question 25. Physical exam is performed on a newborn female due to abnormalities detected at birth.

Newborn has dry skin, swelling around the eyes, enlargement of the tongue, and an umbilical hernia palpated on exam. What nutritional deficiencies should be suspected in the mother of the newborn? So we should be suspecting an iodine deficiency in the mother. So this newborn has classic symptoms of untreated congenital hypothyroidism. It's also known as cretanism. So she has macroglossia, which is the enlarged tongue, umbilical hernia, facial edema, dry skin. They're all classic findings. And in developing countries, the most common cause is lack of maternal iodine intake.

Here in the U.S. is pretty uncommon, like I mentioned before, because we have, not only do I have screening programs, but we have iodine added to our salt and plenty of other. food so iodine deficiency is not common here. Question 26, 37-year-old female presents to the office today complaining of persistent fatigue combined with nausea, generalized abdominal pain, and a brownish discoloration on her hands, elbows, and knees. Labs are ordered and reveal elevated serum potassium levels and a blood glucose of 63. What is the likely diagnosis in this patient? So that's going to be primary adrenocortical insufficiency, also known as Addison's disease. This patient has chronic adrenocortical insufficiency, which is evident by the fatigue,

the nonspecific GI complaints, hyperpigmentation of the skin, hypercalemia and hypoglycemia, which are found on labs. And then the question is, though, finally, is this primary or secondary? And the way that we know that it's primary is the hyperpigmentation of the skin and hypercalemia, which are generally only seen in primary or addicins, but not in secondary. follow-up question question 27 would the ac t h levels in the previously discussed patient be elevated or decreased so remember the patient the last vignette had addisons aka primary adrenocortical insufficiency so they're going to be elevated so primary adrenal cortical insufficiency or adescence disease is due to adrenal gland destruction meaning the adrenal is not producing enough cortisol also aldosterone and this leads to increase aceth pituitary is trying to increase in secretaries trying to increase in the cortisol level, of course, it's failing, whereas secondary has a decrease ACTAH because it's from pituitary failure. So that leads to decrease ACTA secretion.

Just to follow up on the previous question, the increased ACTA is what causes the hyperpigmentation we see in the skin in Addison's. And then the decrease in aldosterone is what causes those electrolyte abnormalities like hypercalemia, as well as hyponatremia too. So that's why you see those in primary because of the abnormalities with the ACEL. C-T-H and the aldosterone. Question 28, a 36-year-old female presents to the office complaining of fatigue, constantly feeling cold, dry skin, and weight gain. If thyroid hormone levels were drawn in this patient, what were the levels of T-SH and free T-4 likely reveal?

So that is going to be an elevated T-SH and decreased free T-4. Classic symptoms of hypothyroidism, fatigue, weight gain, cold intolerance, dry skin. And in hypothyroidism, we know the classic lab findings are going to be an elevation in the T-SH and a decreased free T4. Question 29. Patient with hypothyroidism comes in for routine follow-up and to review labs she had done to evaluate her thyroid hormone levels. She takes 50 micrograms of levo-thyroxine daily and has been on this dose for the last

nine years with no issues. Labs come back indicating she is biochemically hypothyroidism. Her TSA is 11. Remember, the normal range is about 0.45 to 4.5. She states she has not made any changes since the last visit and assures you that she always takes for levo thyroxine first thing in the morning, waits an hour before eating or taking any other pills. She's not started any new prescription medications, just an over-the-counter med she started a few weeks ago for some heartburns she'd been experiencing. What is the likely cause of this patient's

sudden increase in TSA? So that's going to be the heartburn medication. So the over-the-counter med she's taken for her stomach, whether it's a PPI and an acid. Levo-thiroxine requires an acidic environment to be effectively absorbed. That's why we don't do it with food or other pills. And as we know, PPI and acids reduce or neutralize the acid in the stomach. So while other pills you can take within an hour, you know, your other cholesterol meds or your blood pressure medications, PPI as well as some in acids, vitamins, calcium actually need a four-hour buffer period. So while she thinks everything's fine, she's doing what she normally does,

she's waiting an hour before taking this PPI, certain medications and supplements like PPI's, calcium, iron, actually need a four-hour buffer period. And that's what's causing the increased TSA we see in this patient. So certain meds remember need four hours rather than just the hour we see with most medications. Question 30, a 47-year-old female has recently started methamazole for treatment of Graves disease. She often feels very jittery, anxious, and sometimes feels as if her heart is beating out of her chest. In addition to methamazole, well, medication class can be used in this patient to rapidly improve her symptoms.

So that would be beta blockers, propranololol, telololol. beta blockers alleviate the symptoms of hyperthyroidism that are caused by that increased beta adrenergic tone. So symptoms like tachycardia, those palpitations, anxiety, they can all potentially be eliminated or at least improved with beta blockers. Question 31. What would be the first line medication to use in a patient with acromegaly due to a pituitary adenoma? So the first line medication is going to be a somatostatin analog. So that's going to be ocriatide most commonly. Another one is known as lanreotide.

So somatostatin inhibits the release of growth hormone. That's why we use those somatostatin analogs. Question 32, a 42-year-old male presents to the office complaining of decreased libido and erectile dysfunction. He has a history of type 2 diabetes, hypertension, hyperlipidemia, and bipolar disorder, and his medications include Zocor, amylopin, metformin, and respiridone. Labs are drawn which reveal an elevated prolactin level. What would be the first-line treatment option for this patient? So first line treatment option for this patient is going to be discontinue the offending agent, which in this case is going to be the respiradone that he takes. So this patient has hyperprolactinemia and the cause is the respiridone he's taking.

So respiridone as well as other dopamine antagonists like heliparidol can lead to hyperprolactinia. And the reason is because these agents are dopamine antagonists. So they block the effective dopamine. And what does dopamine do? It's an inhibitor of prolactin. So decreased dopamine, more prolactin, and it can lead to hyperplatin. lead to hyperprolactenemia like we see in this patient, and the first line management will be to discontinue the respiradone and switch is something different for his bipolar disorder.

Question 33. Well, medication can be used in a patient with primary hyperparathyroidism to lower serum calcium and serum ptch levels. That is not a candidate for surgery. So that medication is something known as synachalcocet. It's a calciumimimetic. It works by lowering the parathyroid hormone levels by increasing the sensitivity of calcium sensing receptor. So kind of tricks the body into thinking there's more calcium floating around than there actually is. So it doesn't produce as much PTH and therefore you're going to produce less calcium. And remember, if a patient has osteoporosis, another medication class we can use in patients

with primary hyperparathyroidism is bisphosphonates. Question 34, patient with a history of type 1 diabetes presents with tachycardia, weakness, altered mental status, and fruity or acetone. breath. Finger stick is done bedside, which reveals a blood glucose of 560, and his urine is positive for ketones. On physical exam, you know deep, rapid, and labored breathing. These respirations are a compensatory mechanism for what acid-based disorder that is likely present in this patient. So the acid-based disorder that's likely present in this patient would be a high anti-gap metabolic acidosis. Just remember that DCA is the D in mud pilers that we talked about in the mnemonic for all those

acid-based, all the high anti-gap metabolic acidosis. So this patient has what's known as Kuzmal respirations. It's a compensatory mechanism for the metabolic acidosis as the patient's experiencing. It's his body's way of trying to increase the rate and the depth of respiration to blow off more excess CO2. Question 35, patient presents to the ER after sustaining a head injury in a motor vehicle accident. Since the accident, he has been urinating more frequently than normal and has developed an insatiable thirst. His urine is dilute and a finger stick blood glucose reading was 98. What is the first line treatment for the likely diagnosis in this patient?

It's kind of a tough one. But it's going to be desmopressin. So he has polyurea, polydipsyia, sudden presentation should be suspecting diabetes insipidus. So they tell you the urine is dilute. The blood glucose is normal. So you can kind of rule out diabetes mellitus. And also just because of the rapid onset, you should kind of rule out diabetes. But also they tell you the finger stick is normal.

So now we just need to decide is the central or nephrogenic. And they don't give you the results of a desmopressant stimulation test. So you just have to go by the history. So the patient's presenting with these symptoms after a head injury. And that's one of the causes of central diabetes insipitous. And so not only does it lead to central diabetes insipitous, we can kind of rule out a nephrogenic because they don't mention any medications that could have potentially caused it, any electrolyte abnormality.

So we wouldn't really be suspecting nephrogenic. They specifically state that head injury, so we know the most likely diagnosis is central diabetes insipidus, and the first line treatment for that is going to be desmopressin. Question 36, 46-year-old male is diagnosed with S-I-A-D-H. He has a history of seizures, asthma, hypothyroidism, and hyperlipidemia, and is taking a torvastatin, levolyroxine, albuterol inhaler, lovaza, and carbamazepine. This continuation of which medication is recommended in this patient. So remember again, he's taking levolyphyrgynyxin, albohyne. Thyroxime, atorvastatin, albuterol, lovaza, and carbamazepine. So the med you're going to stop is going to be carbamazepine.

So almost all anticonvulsants have the potential to cause S-I-A-D-H, and carbamazepine in particular is the one that seems to be a popular one to ask about. So other medications, hydrochlorothysidesides, some SSRIs, IV cyclofosophomide. They can all predispose a patient S-I-D-H, but definitely remember carbamazepamines as well as your other anticonvulsants. Question 37, what screening test should be done annually for diabetic patients to screen for early signs of diabetic nephropathy? So that would be a urinary albumin, also known as another test for that is a spot urinary albumin to creatin ratio. So albumin is a protein that's usually too large to get through a healthy function in kidney. Once the kidney starts to get damaged and like in diabetic nephropathy, it's no longer able to retain the albumin back into the body. So we start to see it spill out into the urine.

and it's an early sign of diabetic nephropathy. So you're looking for any increase above 30 in the urinary albumin. Used to be called, and probably the term you're familiar with is microalbinuria. It's not called called that anymore. From 30 to 300, that's called moderately increased albinuria. And then anything above 300 is called severely increased albinuria. Question 38, what is the most common cause of diabetic ketoacidosis? So most common cause of DCA is going to be infection like pneumonia, UTI.

It's going to be your most common cause. just due to the counter-regulatory hormones like epinephrine that predispose these patients to D-K-A. Question 39, the patient with hypokalcemia has contraction of facial muscles provoked by lightly tapping on the facial nerve just anterior to the ear. What is this known as? So this is going to be known as the Vostek sign. Vostek sign, which is spelled C-H-V-O-S-T-E-K sign. Question 40, a 64-year-old female with history of type 2 diabetes.

presents the office due to her blood glucose running higher for the past few months. She's made dietary changes as well as increasing her activity level with no improvement in her blood glucose readings. She agrees to add another medication to her regimen and you discuss a few medications with her, including epigliflozine, laryglotide, and glypid. She states her only requirement is that the medication will not cause her to gain weight. Which of these three medications discussed should be avoided? So if you don't want her to gain weight, which matter you're going to avoid? remember the med options were mpigliflozin, loraglatide, and glypizide, which one are you going to avoid? So it's going to be glypizide.

So glypizide is a sulfonioria. It can cause weight gain. The other two listed laryglotide is a glp1 receptor agonist. That actually causes weight loss. Actually, a couple of the glpfewan receptor agonists have been turned into weight loss meds. They're rebranded, so those are really good weight loss meds. So definitely not a laryglatide. And then mpigliflosen, it's an SGL2 inhibitor.

It can also cause weight loss. So the only one, one in these three meds is that's going to cause weight gain is glypozyme. The way that I used to remember that is that I used to remember the sentence, if you sit too much, you can get fat, like in PA school. So if you sit too much, you can get fat and then sit stands for the three classes of diabetes meds that cause weight gain. That's going to be sulfonurias, insulin and TZDs. TZDs, remember, like rosy glitazone, so those are the only ones that cause weight gain and diabetes. All of the other ones are either weight neutral or can cause weight loss. So if you sit too much, you can get fat, sulfoniorias,

insulin TZD classes. Question 41. What diagnosis should be ruled out in a patient who has a radioactive iodine uptake scan of the thyroid perform that shows little to no iodine uptake, which is also known as a cold nodule. What should you rule out in this patient? That's going to be a malignancy. So these patients need further testing to rule out malignancy with normally a fine needle

aspiration. Still really rare even in a cold nodule to see a thyroid malignancy only about 5%. But you do need to roll that out in a cold nodule. Question 42, a 46-year-old male with the history of inflammatory bowel disease, hyperlipedemia, pancreatitis, renal failure, and trigeminal neuralgia is going to be started on metformin for his newly diagnosed type 2 diabetes. Which medical condition listed in his history would be a contraindication for starting metformin. Remember again, he has inflammatory bowel disease, hyperlipedemia, pancreatitis, renal failure, and trigeminal neuralgia. The one medical condition that's listed that would be a contraindication would be renal failure. Remember, due to the risk of lactic acidosis with metformin, we don't start patients with renal failure on metformin.

Normally, the GFR cutoff is going to be less than 30 where it's absolutely contraindicated. Question 43, what is the most common cause of hyperthyroidism? So hyperthyroidism most common cause. It's going to be Graves disease. Question 44, 46-year-old female presents to the emergency department because she feels like her heart is beating out of her chest, and she's also complaining of a persistent headache. On exam, she is diaphoretic, has a pulse of 122, and a blood pressure of 162 over 108. Her labs show that her plasma fractionated metanephrine's are significantly elevated. A CT of the head, abdomen, and pelvis are performed and discover a mass.

For the likely diagnosis in this patient, where would the mass most commonly be located? So that would be the adrenals. This patient has a feochromachycinoma, which is evident by the classic triad of a headache, sweating, tachycardic, as well as being hypertensive, which is another key finding. And then, of course, the elevated metinephrine. So since a feochromosytoma is a catacolamine secreting adrenal tumor, the mask that we did on imaging on the CT would be found on the adrenals. So that would be the area we would see on the CT. Question 45, 67-year-old male with the history of type 2 diabetes presents to the office today complaining of shortness of breath

that is increasingly getting worse. He's also known. noted some unexplained weight gain as well swelling in his lower legs. On physical exam pitting edema is noted in the lower extremity and rails are auscultated at the lung bases. He started out on a new oral diabetes medication a few months ago by his endocrinologist, but he cannot remember the name. Which class of diabetes medication was he likely started on that led to his current presentation? So that's going to be the TZD class, which is going to be a thiozolidindione.

It's the reason why we call it the TZD class. That's going to be your rosy glitazone, your pia golytosome. So these meds can cause or exacerbate congestive heart failure and actually carry a black box warning for CHF. Another reason why these meds are not commonly used anymore. Question 46, 45-year-old male presents to the office complaining that his wedding band no longer seems to fit and some of his hats seem to be too small. He also complains of headaches as well as some visual changes. What would the initial test of choice be for this patient to screen for the likely diet? diagnosis. So the screening test we would do is insulin-like growth factor, also known as serum

IGF1. So this patient has a clear presentation for acromegaly, which is caused from a growth hormone secreting pituitary adenoma, which is also known as somatotroph adenoma. So we measure the serum IGF concentrations because they're elevated in virtually all patients with acromegaly, and they provide excellent discrimination from normal individuals. Remember the actual name of the disease is based all upon whether or not the epiphypul plate in the bone is closed yet. So in adults, it's obviously closed. We call it acromegaly. In children, it's not yet closed.

We call it gigantism. Same thing. Different name just due to the epiphypacal plate closure. And then I used to remember that because acromegaly starts with an egg. So that helps me remember A adults acromegaly. Question 47, a 72-year-old female presents to the office today for a routine checkup. She forgot to bring her medication list, but says she was started on a new medication. for diabetes. She said all she can remember about the medication is that it's supposed to flush

the glucose out through her urine. Which class of medication is this patient likely taking? So that would be an SGLT2 inhibitor like Epiglozin, Kanicalflosen, and those medications flush the excess glucose out through the urine. Question 48 was the most common cause of primary hyperparathyroidism. Most common cause of primary hyperparathyroidism is going to be a parathyroid adenoma. Question 49. 86-year-old female is brought to the ER today by rescue. She was found in her apartment unconscious by a neighbor who called 911. On exam, her pulse is 46. Her blood pressure is 82 over 52, and lab findings reveal her free T4 levels are so low they are undetectable. Family member who accompanies the patient at a state she normally has a nurse who comes to the house

each day to dispense her medications, but unbeknownst to the family, she has not showed up for over three weeks. What medication was this patient likely taking daily prior to a nurse not showing up? So that would be lebo-thyroxine or synthroid, or any other thyroid hormone replacements, really. This patient has what's known as mixed edema coma. It's an extreme form of hypothyroidism. That's evident in this patient due to the bradycardia, hypotension, extremely low free T4 levels. And these patients can also have hypothermia, hypoglycemia. It's generally seen in elderly patients. Sometimes it can be patients who are noncompliant with their thyroid hormones. hormones, but really the most common causes are going to be some acute precipitating event like

MI or infection. Question 50, 36-year-old female presents to the office complaining of fatigue, polyurea, and recurrent candideal infections. Screening for what condition should be performed in this patient. So that would be screening for diabetes mellitis. So fatigue, polyurea, all very common to patients with diabetes, but then the key is that recurrent candideal infections, which are common in diabetic patients due to the increased glucose in the urine. So glucose promotes adhesion of candida to either the vaginal epithelium or the bucumicosia, which can impair phagocytosis. It can lead to recurrent vulvovaginal, candidiasis, or even thrush. All right, that was it. Question 50. We are done. I hope that was helpful. Please let me know if it's helping you in the comments. And I thank you so much for

listening to my podcast and thank you so much for the support. And good luck in PA school. Good luck and your pants, your penury, and your EORs.