INI SS April 2026 Recall: Endocrinology

[00:00:00]So today we'll be discussing the recalls from the April 2026 INASS session. Now if we look at the overall exam pattern, there were a lot of oneliners, not many case-based MCQs and there were absolutely no image based MCQs from the endocrinology section. Now if we look at the topic distribution u the newer part was that from diabetes section there were lot of updates I think which was very new. Generally INASS does not have a lot of MCQs from the diabetes section.

[00:00:29]Especially there were a lot of MCQs from the lipidology part.

[00:00:36]Along with that in the adrenals there were lot of MCQs from focytoma section and there were very few MCQs from the pituitary section as compared to the previous set exams. So now starting off with the discussion we'll be first discussing the pituitary in terms of pituitary.

[00:00:57]Uh the first question was which of the following is most accurate regarding pituitary incident. So less than 10 mm no monitoring or follow-up required visual field testing only symptoms present hormone testing in all and surgery in all. So if you look at the MCQ section by section first less than 10 mm no monitoring is required this is absolutely false. you still need to follow it up after 2 to 3 years and then more frequently if needed. Uh in terms of visual field testing done only if symptoms are present. This is false. We also need to do visual field testing if the adinoma is near to the optic kaisma or it is impinging on the optic kaisma optic tract. Hormone testing is required in all surgery in all. This is again false. We need to do surgery only if there are absolute indications for surgery. So the indications for surgery are visual compromise tumor which is secretreting hormone.

[00:02:09]If there is any other emergency like pituitary epoplexy or if there is rapid enlargement in the size of tumor on followup.

[00:02:22]So they have asked what is true there is only one option which is true that is hormone testing is required in all. So only indications for surgery are visual compromise if on followup there is significant growth of the tumor hormone production or if there is a pituitary emergency like an epoplexy.

[00:02:40]So true is option number C. Now moving on to the next option. So this here they are asking regarding immune checkpoint inhibitor therapy. So now first off in terms of immune checkpoint inhibitor therapy CTL4 inhibitors are more commonly associated with hypopiesitis as compared to PD1 PDL1 inhibitors.

[00:03:03]Now this is mainly uh attacking the center of your pituitary. So ACT deficiency is the most common and it will cause pituitary enlargement and because of pituitary enlargement there can often be visual compromise also.

[00:03:17]There is no hyper prolactinmia and there is no AP deficiency because this is isolated adino hypophasitis. There is no involvement of the stock or the posterior pituitary. So now let us go through MCQ options one by one. And what is not true? So CTL4 inhibitors cause panhypeterism with pituitary enlargement. This is true. PD1 inhibitor most commonly cause ACT deficiency. So yes definitely center of the pituitary is involved. So ACT is the most common hormone which is involved in immune checkpoint inhibitor hypopitis. So this is true. Secondary hypothyroidism is most common. This is false. It is act deficiency which is most common. And CTL4 inhibitors are more implicated in hypophasitis than PD1 inhibitor. So this is absolutely true. So the option which we have to choose is option C. So overall incidence of immune checkpoint inhibitor hypophasitis is 17%age. Mean age is around 60 years. Why? Because this is mainly used in oncology patients and mean age of oncology patients is also higher. Now mean time to hypoitis is 10.5 weeks with CTLA4 inhibitors. It is longer with PD1 PDL1 inhibitors. It is 27 weeks. Uh it is more commonly seen in males as compared to females. Center of the pituitary is involved. So two hormones which are present in the center of the pituitary that is act and DSH. So ACT deficiency is most common followed by DSA deficiency and AP deficiency in hyperpolaria is not seen because there is no involvement of the stock and there is no involvement of the posterior reputatory now. So the option is option number C.

[00:04:59]Now moving on to the next MCQ. So here they are asking for SSTR expression and its correlation with hormonal secretion.

[00:05:07]So select the correct statement regarding receptor expression. SSTR1 with DSH adinoma. SSTR2 with resistant Cushing disease with hypoglycemia. SSTR5 commonly associated with ACD dependent Cushing disease and pandopaminergic agonism decrease size in acromegali. So let us uh understand it one by one.

[00:05:29]SSTR2 expression is mainly seen in densely granulated somatropinoma and it is seen in TSH.

[00:05:42]SSTR 5 expression is seen in sparssely granulated somatropinoma and it is seen in majority of the cases with Cushings disease and dopamine receptor expression is mainly seen in patients with prolactinoma. So this is the usual pattern. So if we look at the MCQs now I think the option is very clear. SSTR5 commonly associated with ACT dependent questions. Now let us look at the other options. TSH adinoma here it should be SSTR2. Uh resistant Cushings disease with hypoglycemia it should be SSTR5 and pandopaminergic agonism this is mainly seen with prolactinoma. So the correct answer is option number C. So moving on to the next MCQ. A patient with bipolar disorder on lithium develops diabetes incipidus. Which is the mechanism of action? So here it is a straightforward MCQ asking on the mechanism of action.

[00:06:40]Now in terms of lithium and its association with endocrinology most commonly what we see is hypothyroidism or goer enlargement or goer formation which is seen uh most commonly associated with lithium use. So here this is mainly seen in females with anti-TPO positivity. Then it can be seen with prolonged lithium use for a long period of time. Second we see association with hypercalcemia or hyperarathyroidism.

[00:07:25]And here again the mechanism is lithium resets the set point for CSR. So the set point for CSR is reset. So that is why there is increase in PTH secretion and this increase in PTH secretion for a long period of time can cause development of parathyroid adenoma and downstream it can cause hypercalcemia. And the third common disorder associated with lithium use is AVP resistance. Now here the mechanism of action is that lithium enters into the uh tubules through the enac channel within the tubules it will cause reduction in CM production and because of this reduction in CMP production there is reduction in aquaporin to expression. So what is the mechanism of action? Decreased aquaporin channel production entry through inac channel is also true but that is not the mechanism for AP resistance. So the correct answer is decreased aquaporin channel production. Now hypothyroidism is seen in 10 to 20%age. Uh subclinical involvement is seen in 30 to 40%age.

[00:08:35]Goer is seen in 40 to 50%age. Risk factors are female sex and positivity and prolonged use of lithium. uh here it will be causing inhibition of preformed thyroid hormone release. It will be also causing reduction in iodyroine coupling and there will be decreased thyroid sensitivity to TSF and it can also unmask autoimmune thyroiditis.

[00:08:59]Now in terms of hypercalcemia and hyperarathyroidism this is seen in 5 to 10 percentage in overt and hypercalcemia overall is seen in 10 to 25%. Now here the mechanism is raising the CSR set point which will cause increase in PTH.

[00:09:15]Chronic increase in PTH can also cause adinoma formation and mostly there is mild hypercalcemia with slight increase in PTH value. Next is AP resistance.

[00:09:26]Again this is entry into the collecting duct into the tubules through the ENAC.

[00:09:31]Here there will be reduction in CM and this reduction in CM will cause down reggulation of aquaporin 2 expression and this is what will cause AP deficiency. So the treatment is to block the entry of lithium into the enac. So for that we use amoride.

[00:09:53]So the correct option is option B.

[00:09:56]Now moving on to the next MCQ somatin analog used in Cushing syndrome associated with worsening of hypoglycemia. So switch off metformin to basilbas insulin which is the likely causitive drug. So now if we look at Cushings the most commonly drug uh used drug in terms of pituitary Cushings is pereotype. Now pereotide acts predominantly at the level of the SSDR5.

[00:10:25]Now the problem with this drug is that on the pancreas beta cells predominantly express SSTR5 while alpha cells predominantly express SSTR2. So what happens with pacerotide is that there is reduction in insulin production along with increase in glucagon production.

[00:10:48]So that is why there is worsening of hypoglycemia seen very commonly with pereotype. So for this MCQ the answer is definitely pereotype. Now in terms of Cushings what is the drug which is used to control Cushings and also it is mainly targeted for glycemic control. So that is my pristone.

[00:11:11]So my pristone is a gluccocorticoid receptor antagonist. Now because it is a gluccocorticoid receptor antagonist it is going to block the gluccocorticoid receptor. So when you send the patient serum cortisol values the serum cortisol values will actually be increased. So how you monitor a patient with Cushings on my pristry you look at whether there is improvement in the glycemic control and whether there is improvement in the blood pressure of the patient. So this is the drug which can be asked with Cushings uh in terms of glycemic control. Now in terms of acromagali with octriotide in patients of acrogal with diabetes there's generally improvement in glycemic control which is seen. Why? Because octriotide is predominantly acting on the SSTR2. It is also acting on the SSTR5. But when you use octriotide in a patient with acrogali there will be reduction in the growth hormone burden. And this reduction in the growth hormone burden will cause improvement in glycemic control. And while it has some action on SSTR5 also but this reduction in the burden of growth hormone will predominate over its action weak action on the beta cells. Now in a patient without pre-existing diabetes there can be some increase in incidence of hypoglycemia but this is seen only in 15 to 20%age of individuals. Why? Because octootide while it acts on the SSDR2 it also acts on the SSDR5. So there will be reduction in glucagon along with reduction in insulin and in some cases this can cause hypoglycemia. While with piraotide this is a lot more common almost seen in 50 to 55%age of cases. It appears within 2 weeks of therapy onset and the other side effect associated with SRLs is choleiththasis.

[00:13:08]So here the answer is piotic.

[00:13:10]Now moving on to the next MCQ. Which of the following is not true? CR and AVP both can simulate the corticotroof. This is absolutely true. Both can simulate the corticotroof. Corticotroofes are located in the medial portion of the anterior pituitary. Absolutely true. Two cell lines in the medial portion of the anterior pituitary. They are uh the act cell line and the DS cell line. And gonadotropes are distributed throughout the pituitary. ACT is a hormone with 29 amino acids. So this is absolutely false. It has 39 amino acids. Now along with ACT we generally use two analogs for testing. Number one is sinctin or synthropac or cosinotropen.

[00:13:59]So if any of these words has been used they contain 24 amino acids. So these are the first 24 amino acids which are metabolically active hormonally active from the 39 amino acids. So if the question is asked whether co-signotropine has 24 amino acids that is true. Now the other form which is used for testing uh in terms of the adrenal reserve that is acton prolong atom and this is porsine act and this has exactly 39 amino acids available. So act has 39 amino acids. Cintropac cosinotropin cythin has 24 amino acids which are the first 24 in the 39 amino acid chain and acton prolongatum has 39 amino acids. It is the pick form the porine form and in corticotrope storage vesicles are located close to the margin of plasma membrane. This is true. So what is not true? ACT has 29 amino acids. It actually has 39 amino acids.

[00:15:05]Now moving on to the next section that is adrenal which is not an oral drug for medical adrenal ectomy. So if we look at the medical management of Cushings for patients who are having emergency associated with Cushing disease and who need inhosp management of hypercortisolia in an acute setting. Here the most commonly used drug isomedate. It is used as an IV infusion. Looking at the other options, ketoconazole is an oral drug.

[00:15:36]Mito again is an oral drug. Ocelotrostat is also an oral drug. So which is not an oral drug? That is it.

[00:15:44]So it is in administered intravenously.

[00:15:48]Its efficacy is near 100%age. It is effective as a bridge therapy to surgery. So patient coming to you with acute complications of Cushing. It could be a glycemic crisis. It could be anything. It could be severe infection patient having psychosis. So here you'll use it as a bridge to surgery and then subject the patient to surgery. Oilroat is an oral 11 beta hydroxilase inhibitor. Along with that it also inhibits aldoststerone synthesis and mitoin it is an adrenolytic agent. So it is often used in patients with ACC along with Cushings. So which is not an oral drug it is which is given IV. So patient with adrenal focytoma elevated metronfrine levels and medularary thyroid cancer what cluster do they belong to? So here they are trying to say that this patient has men two. So what is the cluster for men two? So remember for fio there are three clusters cluster one 2 and three. Cluster one is further divided into 1 a and 1 b. Now here if there is involvement of the crab cycle you call it as cluster 1 A. If there is no involvement of the crab cycle but still there is the pseudo hypoxia pathway which is involved you call it as cluster 1B. Cluster two has mainly involvement of the kynis pathway and cluster three mainly has involvement of the WT pathway. Now cluster one is predominantly going to be secretreting nor metaninephrine or nor adrenaline.

[00:17:26]Cluster two is predominantly going to be secretreting epinephrine, adrenaline or metinephrine. And cluster three again has mixed pattern of involvement. In terms of cluster one also cluster 1 A will be having secretion of dopamine plus norinephrine. Cluster 1 B will be purely norinephrine secretreting and cluster two in most cases is isolated there is secretion of metaninephrine or adrenaline while cluster three has a mixed pattern. So now which are the genes involved in cluster 1 A. Cluster 1 A has predominantly involvement of the SDH pathway. Cluster 1 B has predominantly involvement of the VHL pathway, the EPAS pathway or the HIF2 alpha pathway.

[00:18:13]While cluster two has all the men. So men uh two that is the men 2 involvement. It can also have men five that is involvement of the max mutation and it can also be seen with NF1. So NF1 is the exception where it is part of the cluster 2 pathway but still it is norminephrine secretreting. So here if we move on to our MCQ MTC with elevated metaninephrine. So even with elevated metaninephrine you can suspect that the answer will likely be cluster two only and further with medularary thyroid cancer it confirms it is meant to so cluster 2 mutation.

[00:18:59]Now the most common tumor associated with SDHB mutation. So again uh if we look at the syndromes associated with uh mutations in fiochromosytoma we can look at the SDHB pathway. Now SDHB pathway has increase in incident of a lot of cancers. So those two predominantly that is gist and renal cell cancer. Now here for renal cell cancer overall RCC is more common than just in terms of SDHB mutation pathway.

[00:19:29]But in terms of RCC it can be clear cell RCC or it can be just normal common garden RCC. So here overall RCC is more common than gist. But if we look at the clear cell variant gist is more common than clear cell variant of RCC. So uh in terms of recall I think a few of the students have suggested that it was specifically mentioned clear cell RCC.

[00:19:57]If clear cell RCC was specifically mentioned then gist will be the answer.

[00:20:01]If overall only RCC was mentioned then RCC is more common than just and RCC will be the answer. Now what you need to remember here is that VHL is also often associated with clear cell RCC. Now in terms of the other involvements in patients uh with fiochromosytoma or paragloma polyythemeia may be associated with epas mutation it can be associated with pdh1 and pdh also. Now in terms of uh hif2 alpha there is paragangloma with polyythemeia with somatinoma.

[00:20:41]Now uh reed syndrome is seen with fummerate hydroase mutation and here there are uterine fibroids RCC with hereditly leommyometosis and there is multif focal and metastatic fiochromosytoma paragangloma. So what you need to remember in terms of syndromes associated with fiochromosytoma number one with uh SDH mutation there can be associated just there can be associated RCC. RCC might also be seen along with VHL and especially it can also be seen associated with REIT syndrome. Now Reed syndrome is because of humorate hydrated mutation along with RCC it has uterine fibroids. Now in terms of polyythemeia, polyythemeia can be seen with HIF2 alpha mutation, PDH1, PDH2 in HIF2 alpha mutation associated with polyythemeia there can be presence of somatinoma also. So this is probably what you need to remember in terms of association of fiochromosytoma and paragloma. Now what is true regarding biochemical assessment of focytoma?

[00:21:49]Urine metinephrine, urine epinephrine and norepinephrine are measured as it is produced continuously. This is not true.

[00:21:56]Epinephrine and norepinephrine can often have intermittent secretion.

[00:22:01]Now because they have intermittent secretion, these epinephrine and norinephrine, norepinephrine further get converted to metanphrine and norinephrine.

[00:22:12]So metaninephrine and nor metaninephrine are downstream metabolic products of epinephrine and noran norepinephrine and they are produced continuously.

[00:22:23]So that is why we always use metaninephrine and nor metaninephrine essays for diagnosis of fo or paragrangloma. Why?

[00:22:33]Because they are produced continuously.

[00:22:34]They have a constant level in your body and metanphrines are secreted immediately from the tumor. Again they are not secreted from the tumor. They are downstream products. What is secreted from the tumor is either epinephrine or non-epinephrine. They get metabolized by enzyme called COOMT into metinephrine. So they are not secreted from the tumor. So only thing which is true true is urine metinephrine and noranphrine are produced continuously by COOMT and they are used for assessment of focytoma.

[00:23:06]So the correct answer is option B. Now moving on to the next MCQ. Which of the following is not a treatment option for metastatic fio or paragloma? Now remember for metastatic fio or paragloma what are the options that you have? Number one you can go for tumor debulking. After tumor debulking has been done and there is residual or if the tumor debulking is not possible then the options that you have are chemotherapy. In terms of chemotherapy what we can use is CVD that is cycloposphomide vin christristine dharas. Next option that we have is I131 MIBG. So MIBG is specifically localized to the adrenals and here it can be used in metastatic fior paragangloma.

[00:23:55]then we can use luteesium based PRRT therapy and rarely you can use further options like teosolomide. So these are what are the options you have for management of a metastatic fio. So PRT is an option resection is an option. I1 131 MIBG is also an option. What is not an option is EDP regimen. EDP regimen is used in ACC.

[00:24:22]It is also known as everbush regimen.

[00:24:27]What is the other named protocol in endocrinology? So that is the st protocol. So where is st protocol used?

[00:24:35]It is used in aggressive pituitary adinomas.

[00:24:42]Here teosolomide is used cyclically for 5 days out of every 28 days. and along with that combined with it concurrent radiotherapy is given. So concurrent fractionated RT along with teosolomide for six cycles followed by just teosolomide is called a step protocol. It is used in aggressive pituitary adinoma and endocrinology.

[00:25:08]Otherwise, it is also used in other brain tumors like glyobblastoma.

[00:25:19]So here the answer is EDP regimen. It is used in ACC. It is not used in fiochromocytoma.

[00:25:25]So a 65 year old patient presenting with resistant hypertension having adrenal mass of 1.2 2 cm on both sides with lateralization index and contraateral suppression index which is given. So here what they are asking for is primary ardosteranism in that you're subjecting the patient to AVS. So how do you approach a patient on AVS? First thing which you need to look out for is the selectivity index. So in the selectivity index what you are ensuring is whether the canula has reached up till the adrenal vein or not.

[00:26:00]So here you will look out for the ratio of c cortisol from the adrenal vein divide it by cortisol from the IVC and if this is more than five that means that you are predominantly in an area where the cortisol is very very high. So that means you are in the adrenal vein itself. So first step in interpretation of AVS look out for selectivity index which is more than five. After that you look out for the lateralization index.

[00:26:28]So whatever adrenal gland you are which is dominant. So you uh look at the ratio of aldoststerone divide by cortisol on both the right side and left side. So whichever is higher you divide it by whichever is lower.

[00:26:44]Now if this is more than four so the higher one that is definitely having an adinoma. If this is less than three so that means that both the sides they have almost equal production of aldoststerone. So likely there is presence of bilateral adrenal hyperplasia and 3 to four there is the gray. So here lateralization index of less than three that means that likely the patient is having bilateral adrenal hyperlasia. Now if the lateralization index is between 3 to four then you need to look out for the contrlateral suppression index. So what is the contrateral suppression index? So whenever there is an adrenal adinoma if it is actually very dominant it is going to suppress the adrenal gland on the opposite side. So if you look at the adrenal by aldoststerone by cortisol ratio of the lower one divided by aldoststerone by cortisol ratio from the IVC. So the suppressed adrenal gland should be having lesser aldoststerone production as compared to IVC which is having aldoststerone from both the adrenal glands. So here if it is less than.5 then you can think that the contrateral adrenal gland is suppressed.

[00:27:58]So if the lateralization index is between 3 to four. So if it is in the gray zone then you look out for other supportive evidence and in terms of the supportive evidence if the contrateral suppress suppression index is if that is less than.5 that means that the opposite adrenal gland is suppressed and uh whichever side the a by c is higher that is having an adinoma which is suppressing the side on which the ardoststerone by cortisol ratio is lower. So here if the lateralization index is less than three you don't need to look out for the contrlateral suppression index also. So for this question you don't need to see the contrlateral suppression index but if say the value was 3.4 4 then you need to check out the contrlateral suppression index and if the contrlateral suppression index is less than 0.5 that means that there is an adinoma here in this MCQ the contrlateral suppression index is also more than.5 that means that again this is also supportive of a bilateral adrenal hyperplasia so selectivity index confirm successful adrenal vein canulation you look out for cortisol in the adrenal vein divided by cortisol in IVC alternative markers which you can use are 170 HP and endrostand.

[00:29:15]Next is the lateralization index. You look out for A by C on the dominant side divided by A by C on the non-dominant side. If it is more than point greater than four, it suggests unilateral disease. Less than three, it suggests bilateral adrenal hyperplasia. Between 3 to four is the gray zone and you need to assess the contrlateral suppression index. In the contrateral suppression index, you only do it if it li falls in the 3 to4 range. Here if the A by C of the non-dominant side the lower one divided by A by C of the IBC if it is less than.5 it means that there is contraateral separation which is happening from the adinoma. So this confirms an adinoma. If it is more than.5 it means that there is a bilateral adal hyperlasia. So in our MCQ the answer is straightforward bilateral adal hyperlasia consider MRA. Next again an option a question with primary aldoststeroneism I arr suggestive of lateralization towards the left side. Now here if the imaging that is pet city is suggestive of uptake on both the sides which of the following is true. So for the purpose of exam as the gold standard investigation. So anytime there is controversy between AVS versus any imaging modality you'll be looking out for whatever is there on the AVS. So for this MCQ it shows lateralization towards the left side. So you will mark it as unilateral micronodular adrenal adenoma causing hyperardostism and you will subject the patient to surgery. Now in clinical practice I think it is a slightly bit more complicated but here for exam purpose AVS is the gold standard lateralization towards the left. So that means that there is an adinoma on the left side. So if the PET is not picking it up it is still there is a micronodular disease which is causing an edinoma and this is the cause for hyperardostism.

[00:31:17]So the answer is option number A. Now patient having features of hyperpigmentation, salt craving, hyponetri hypercalemia what is likely primary or secondary adrenal insufficiency. So how do you differentiate primary from secondary adrenal insufficiency?

[00:31:34]Primary will be having absence of glucocorticoid, mineralcorticoid and the weaker androgens that is DHEA. So all three will be absent in primary along with that there will be high ACTs. here there will only be deficiency of glucocorticoid and deficiency of the uh adrenal u androgen axis. So this is why they will not be having hyperpigmentation because the act is normal while here because act is high they'll be acting on the MC1 receptor and they will be causing hyperpigmentation and because of mineralotic deficiency there will be lack of aldoststerone which will be causing hypercalemia. So here there will be normal potassium. So a patient presenting with salt craving suggestive of mineralotic deficiency, hypercalemia suggestive of mineralotic deficiency and hyperpigmentation suggestive of excess of ACT. The answer is primary adinary sufficiency or Edison's disease. So what are the therapeutic plasma levels of mitoten? So this is straightforward in information based MCQ ACC you need to maintain it between 14 to 20. In Cushings you can allow lower values of mitoin. So here you can allow 8.5 to 20.

[00:32:52]So here in most cases they are asking for therapeutic plasma levels of mitoin in ACC and the answer is 14 to 20. So in Cushing disease the value which you need to maintain is 8.5 to 20 while for ACC for antitumor effect you need to maintain it between 14 to 20 uh mg per liter.

[00:33:14]Now a patient presenting to you with adrenal tumor with size which is more than 4 cm. So size of 6 cm attenuation which is more than 20 houndsful units.

[00:33:24]So you need to suspect either FO or ACC for this patient. So you will definitely never be doing FNAC. Why? Because if it is FO it can precimitate fiochromosytoma crisis. If it is ACC it can seed the tract and if it can seed the tract there can be progression of disease for ACC.

[00:33:46]So what is incorrect? FNAC is never to be done. Assessment of metinephrine nor metaninephrine all patients with adrenal incidental require assessment of metaninephrine and nor metaninephrine.

[00:33:58]So this is true. FGDG PET should be considered. Definitely true. O and DST should be done in all.

[00:34:08]So moving on to the bone section.

[00:34:10]Patient with thyroid surgery presenting with hypocalcemia. Which of the following is least useful? So this is a case of post-operative hypoparathyroidism.

[00:34:23]The risk factor for post-operative hypoparathyroidism is PTH less than 10 on after the in the first week postoperatively. So here you treat it with calcium supplementation and calcid.

[00:34:39]Now if the calcium requirement is more than two, calcid requirement is more than 2 micro g per day or here calcium elemental calcium requirement is more than 2 g per day then you should you should consider using PTH analog that is recombinant RPT including teriparatide in that subset of individuals. So definitely recombinant PTH is useful. So when you are using calcitrol and if the patient is having elevated urinary calcium you should be starting the patient on thioide to reduce the calcium excretion from the patient. So thioide is useful in hypercalceura on therapy and often because of low PTH it can cause magnesium deficiency. So oral magnesium should be used. So these three options are definitely useful. What is least useful is denosomab and of course a patient presenting to you with hypocalcemia denosomab is going to worsen your hypocalcemia. So this is the obvious answer and the answer is denosomab. So denosomab is the only option which reduces calcium. So of course it is not useful in hypocalcemia.

[00:35:51]So when do you consider pt replacement therapy? If there is symptomatic hypocalcemia, if there is hyperphosphate which is difficult to treat. If there is renal insufficiency earlier stages, if there is hypercalceia which is difficult to treat, if there's poor quality of life and especially if the calcium requirement is more than 2 g per day and active vitamin D requirement is more than 2 microgram per day. Now a patient of breast cancer with multiple vertebral fractures. Now remember anytime a patient has multiple vertebral fractures with osteoporosis the treatment of choice is teriparatide. Now terraparatide is contraindicated in active malignancy. So here a patient having breast cancer active malignancy you will not be using teriparatide.

[00:36:40]So the options you are left with are bisphosonates and calcetonin. Calcetonin do not reduce your fracture risk. So there is no reduction in fracture risk with calcetonin. So the only option you are left with is b phosphonate. Now here if the option D was denosumab, denosumab has direct reduction uh some reduction which has been seen in trials in terms of progression of breast cancer.

[00:37:07]Also it has been shown to improve HB1C slightly. So if these were the options say a patient with hypoglycemia or a patient with breast cancer and if denosummap was the option mentioned here then we would have chosen denosomapab but denosomab is not given as the option so the only option that we are left with are bisphosphonates. So the answers are bisphosphonates and if denosomab option was given market as denosomab now 70 year old female this is a slightly controversial question. So uh patient presenting with primary hyperarathyroidism not willing for surgery history reveals osteoporosis and multiple fracture fragility fractures. So what is the treatment of choice? So if we look at uh the data which is available uh what can be the possible answer is that you may be using calcium like synakal set to reduce the PTH values but this reduction in PTH value does not improve um at all the osteoporosis part. It will only cause some improvement in the calcium levels. So cena should only be used if calcium is above 11. Now then in terms of uh treatment of fragility fractures what is the best option? So definitely the best option is denosomap.

[00:38:35]So here calcium values are not given.

[00:38:38]Patient has multiple fragility fractures. Uh so ideal you should be marking denosomap.

[00:38:46]Now the other option which you can mark is also calcium with bisphosphonate. But if this is the accurate recall which has been given and if denosomab is one option and other option is calcatic with bisphosphonate ideally you should be mark marking it as denosumab because calcium levels are not given. So if we look at the PHPT guidelines also in patients with low bone mass who do not undergo parathyroid surgery we suggest bisphosphonate or denosoma only if the serum calcium levels are above 11 we suggest syncal and even if we look at the denosina study what did the denosina study showed addition of cynical does not improve BMD further. So simply speaking for improvement of BMD like in the present MCQ you have best option is denosomap over bisphosphonate.

[00:39:43]Now here if it was given that the patient has multiple fragility factors and the patient's calcium is 12.2 then I think the ideal option to mark would be calciumic plus bisphosonate. Why? because addition of calcium does not improve the BMD and this was clearly shown in the denosina study. So slightly controversial answer but this is I think what the examiner is asking they are asking you for whether you are aware about the denosina study or not and probably I would be marking the answer as denosum other close differential answer which could be marked is calcium with bisphosphonate.

[00:40:26]What is the mechanism of action of bureosumab? It is a monoconal antibbody against FGF-23.

[00:40:33]Now in terms of page disease what is not true? Does it cause reduction in bone mass? So no. Pages disease is actually associated with increase in bone mass.

[00:40:44]But this increase in bone mass is disorganized. So this disorganized mass will be causing increased fracture along with increase in BMD. So the first option is not true. Most commonly diagnosed as asymptomatic elevation of ALP. This is true. Cardomegal is a common complication with severe skeletal manifestation. Again this is true especially if uh there is widespread skeletal involvement. Osteocaroma is the long-term malignancy associated with it.

[00:41:15]This is also true. So the only thing which is not true is reduction in bone mass because the key pathophysiology is disorganized remodeling. So this will cause increase in BMD but at the microarchitecture level the bone will be disorganized fibrous and weak. So this is why there will be increase in fracture risk while the rest of the options are true. Now what is not true regarding vitamin D? D2 and D3 both have similar physiological action. Absolutely true. Only their source are different.

[00:41:46]Upper limit of vitamin D dose is 60k per day. This is false. Upper limit is 10k international units per day and vitamin D receptor organs are present in most.

[00:41:56]This is absolutely true. So what is false? Upper limit is 60k IU per day. It is 10k IU per day. Elderly smoker presenting to you with a medastinal mass along with hypercalcemia. What is the next step in evaluation? Any patient presenting to you with hypercalcemia?

[00:42:14]First thing you should ideally do is PTH. Unfortunately PTH is not mentioned in the options. So here what they're asking you uh is a patient presenting to you with a likely cancer. Now what is the most common association of hypercalcemia with cancer? Elderly male smoker likely this is small cell lung cancer and this is going to be secretreting PTHrP which is what will cause hypercalcemia of malignancy. So here the answer is PTHP.

[00:42:46]Now a patient of coron's disease after intestinal resection what will happen is that there will be excess of fatty acids in the intestine.

[00:43:01]So this excess of fatty acid in the intestine will bind with the calcium. So there will be reduction in intra luminal calcium. So because of reduction in in intraaluminal calcium there will be increased oxalate absorption. So this increased oxalate will go into the blood from the blood it will go into the kidney and in the kidney it will bind with the calcium and cause formation of calcium oxalate stones.

[00:43:31]So here the answer is calcium oxalate stones which are seen after intestinal resection in a patient with Crohn's disease. Now this was our discussion of bone. Moving on to discussion of thyroid. So case of over hypothyroidism with stable CAD ideal management. Uh anytime question mentions elderly or a stable CAD always remember that you have to go slow and uptight.

[00:44:01]So how slow you start off low at dose of 12.5 to 25 and then you slowly uptight the dose every 4 to 6 weeks. So if we look at the options start at the full dose of 1.6 microgram per kg. This is false because this will put the patient at risk of tearithmia.

[00:44:26]Start at 12.5 to 25 and gradually increase the dose with TSH monitoring every four to 6 weeks. This is correct.

[00:44:33]Give thyroxine loading dose to prevent mixedma. This is false. Again, increased risk of tachiariththmia. And start at 25 to 50 and do early followup at TSH at 2 to 2 weeks. This is not true because TSH will at least take 4 to 6 weeks to enter into plateau.

[00:44:53]Why? because TSH is is dependent on the average exposure of LT4. LT4 has a long halflife of around 6.7 days. And because it has a long halflife of 6.7 days, it will take at least 5 weeks for TSH to plateau at a specific dose. So start at 25 and early followup at 2 weeks. This will again be false. So the only option that you are left with is option B which is the correct one.

[00:45:26]Now a patient 8 9 8y old female presenting on multivitamin therapy for hair fall. What is true with a picture of toxicosis? So again this is definitely biotin interference only. So here what you need to remember is that there are two types of essays. Number one is the sandwich essay and second is the competitive essay.

[00:45:50]So what happens is that this is your streptoidin coated microparticles.

[00:45:58]So anytime the patient is on biotin the biotin will go and bind to the streptovidin. So the detection antibbody that will be biotiniated will not be able to bind with the strapidin and then the antigen will be not be able to bind here and then the signal antibbody will not be able to bind with it and there will be low signal. So this sandwich essay is generally seen with TSH which is a relatively larger molecule. So because this biotinilated antibbody will not be able to bind to streptoidin TSH will be falsely low. Now for competitive acids which are seen with small molecules like T3 and T4 what will happen is that there is streptoidin biotin has gone and bound to this streptoid. Now in terms of competitive assess what is generally seen is that there is a labeled antigen. This labeled antigen will go and bind with the biotiniated antibbody and this is what will be sending the signals. Now this signal will be inversely proportional to the concentration of the detectable the detection antigen which you want to use.

[00:47:12]So there will be this T3 and T4 and then there will be some label T3 and T4. So this labeled T3 and T4 will not be able to bind through its biotinilated antibbody to strepin. So there will be low signal and this low signal will be interpreted as a falsely high value of T3 and T4. So what happens with biotin?

[00:47:36]There will be falsely low TSH and falsely high T3 and T4 which will give the picture of toxyosis.

[00:47:43]So here you can see that there is this labeled antigen. This labeled antigen is not able to bind with the strepid and in competitive essays the signal is inversely proportional to the analyte concentration. So low signal will mean high values of T3 and T4.

[00:48:05]While with the sandwich essay which is used for TSH low signal will mean low value of TSH and the patient will have appearance of toxicosis and just you need to stop biotin for 48 to 72 hours and repeat the TFT and it will be absolutely normal. Now which of the following groups this we have already discussed are more likely to develop lithiuminduced hypothyroidism. So female with positive TPO antibodies this is absolutely correct. Now here if it was also given old man with CKD with prolonged duration of exposure I think this would come as a close second option in terms of the MCQ but definitely highest risk factors are female positive antiTPO antibodies and long duration of exposure. So here female with positive TPO antibodies that would be your correct answer. Now in terms of diabetes and metabolism in the diabetes section the questions are straightforward. What is the mechanism of action of metformin?

[00:49:06]Of course it is decreased hippatic gluconogenesis and this will cause increase in peripheral glucose uptake. Promote glycos ura by acting on proximal tubule.

[00:49:15]This will be seen with SGLT2 inhibitor and delays glucose absorption. This will be seen with alpha gluccoidis inhibitors. DPPP4 inhibitors the mechanism of action is it decreases the d degradation of GLP1. This is absolutely true. It will cause increase in your incretins and this is how it will be acting. A selective SGLT2 inhibitor. This is of course not the mechanism of action. Improving peripheral glucose uptake and utilization. This is seen with metformin. PPR gamma aagonist. This is seen with thioin dindion that is pioazone.

[00:49:50]So again a straightforward MCQ.

[00:49:53]Which drug reduces HB1C as well as cholesterol by binding to bile salts?

[00:49:58]There is only one bile salt inhibitor which is approved for management of diabetes and this is colival. So colum will reduce HB1C and also it will reduce cholesterol by binding to bile salts.

[00:50:11]Which of the following is false for a patient with fasting hypoglycemia? So H SLT2 cause greater reduction of HB1C as compared to metformin. DPPP4 inhibitors do not directly cause hypoglycemia.

[00:50:23]Sulphonile udias have less durability than pyoglyazone and metformin has no immediate impact on glycemic control. So here if you look at MCQ stepwise SGLT2 inhibitors on average cause.5 to 1.2%age reduction in HB1C metformin causes 1 to 1.5%age reduction in HB1C. So SGLT2 cause greater reduction in HB1C. This is false. So this will be your option.

[00:50:50]DPPP4 inhibitors do not directly cause hypoglycemia. This is absolutely true.

[00:50:55]DPPP4 inhibitors act through incretins.

[00:50:58]Increants are only secreted if you're going to be taking something which has carbohydrate in it. So their release is linked to glucose. So they have low risk of hypoglycemia. Sulfonyluras have less durability than pyogazone. This is again true. Sulfonyl uras they will cause beta cell depletion when they are used for a long duration at a high dose.

[00:51:21]Pyoglyazone they do not cause beta cell depletion they cause beta cell preservation. So pyoglyazone will of course be more durable and metformin has no immediate impact on glycemic control.

[00:51:32]This is partially correct. Generally it causes impact on glycemic control after some hours. So option A is what you need to mark. So which of the following is false regarding GLP1 agonis related side effects? Acute pancreatitis can be seen in some cases especially if gallstone disease is coexistent. Thyroid cancer only one specific type of thyroid cancer that is medularary thyroid cancer is seen in rat models with GLP1 agonist and they were the patients having history of MTC they were uh excluded in all of the trials for GLP1 agonist. Alteration of liver enzymes. This is absolutely false.

[00:52:15]Actually GLP1 agonist are approved for management of mass. So they actually improve your liver enzymes. So it is not a side effect with GLP1 agonist. And worsening of diabetic retinopathy as has been seen with insulin. Same way with GLP-1 analoges. With GLP1 agonist what can happen is that there can be sudden improvement in glycemic control and because of this rapid improvement in glycemic control this can cause initial worsening of diabetic retinopathy as has been seen with insulin. So the only option which you need to mark is alteration of liver enzymes. GP1 ano and agon is there treatment of choice for metabolic stato hippatitis. What is false regarding orforgal non-peptide GLP1? It is safe in pregnancy. There is no data available with GLP1 in terms of pregnancy. Whatever data is available, it is inadequate. So none of the guidelines and none of the GLP1 agonists are approved in pregnancy. It causes G GI disturbance. This is seen as a class effect with odd GLP-1 agonist. Oral GLP1 agonist this is definitely true and interaction with SIP 3 A4 again this is true. So the option you need to mark is safe in pregnancy. So oral is non-eptide oral GLP1 agonist remember semaglutide it has snack so this is how it is absorbed here because it is noneptide it is not degraded not degraded in your git. So it does not require snack. So that is why there is no fasting no uh requirement of fasting which is there with orphogon no water intake. So not no specific requirement of taking 100 ml of water as is seen with simlut class effect is diarrhea seen with all the GLP1 agonist. They can all cause diarrhea. They can cause nausea, vomiting. It is metabolized by SIP 3A4. So drug interactions are possible and like all other GLP1 agonist it is contraindicated in pregnancy because of insufficient human data.

[00:54:29]Whatever data is available with GLP1 agonist it suggests that it is safe to use during pregnancy but enough data is not available. So none of the guidelines have mentioned that it is safe in pregnancy. Now highest incidence of insulin resistance and diabetes malitis.

[00:54:45]This is definitely seen with rosoa statin which is the most potent statin and because it is the most potent statin the side effects which are dependent on HMG COA inhibition uh because of this which will be causing reduction in beta cell insulin secretion worsening of peripheral insulin sensitivity and impaired adiponin signaling. This is most common with rosoastatin and it is least with pavastatin also it is low with praastatin.

[00:55:17]So the data for this is available from the Jupiter trial and in the Jupiter trial what was so shown was that for every patient you initiate rosoastatin you are uh able to prevent 93 vascular events and for this prevention of 93 vascular events and prevention of uh this 93 vascular events there are 54 extra cases of diabetes per thousand patient years of treatment.

[00:55:47]So because of the risk benefit ratio you will use rosoasta statatin in patients in whom it is indicated. Now rosoastatin can cause worsening of CKD. So a patient of CKD stage 4 having EGFR of 24 on high dose of atostatin having myopathy with mildly increased CPK. So anytime a patient has myopathy you need to look out for CPK. If CPK is more than four times the upper limit of normal, you need to temporarily stop status. If it is less than four times the upper limit of normal, you need to either shift to alternate day regimen or you need to reduce the dose of statin or you need to shift to a safe safer statin. So for uh the safest statins in terms of uh muscle related adverse events with statins they are all hydrophilic statins. So among hydrophilic statins are praaastatin and rosoa statin and pavastatin.

[00:56:50]Now rosoastitin cannot be used in grade four CKD because it can cause worsening of CKD and it has predominantly R for our renal excretion. So the option you are left with is praastatin right. So if we look at the intolerance pathway I think the uh the font size is very very small but only thing you need to remember is if CPK is more than four times the upper limit of normal stop statin for 4 to 6 weeks. If it is less than four time the upper limits of normal you can shift the patient to alternative therapy. In terms of alternative therapy, hydrophilic statins like rosoa, praa and pithawa, they are water soluble. So they are selective for the liver. While lipopilic statins, they are fat soluble. So they are very commonly distributed into the muscle. So you need to shift over from lipohilic statin to the hydrophilic statin. And here rosoastatin is renally cleared. So associated with rapid loss of eGFR. So it should not be used. So the only option you are left with is praastatin which is a lipid lowering drug causing gallstone. Again straightforward caph question fibbrates. So now what do these fibbrates do? They cause reduction in bile acid synthesis. Because of reduction in bile acid synthesis this cholesterol will go and bind to whatever bile is left and that will cause super saturation of the bile with cholesterol and this can cause cholesterol colostrone. So this is what is seen with fibroids. Now LDL is still high in a patient on BCSK9 inhibitor. So this is a question which they're asking is for familial hyperc cholesterolmia.

[00:58:31]In familial hyper cholesterolmia there can be homozygous variant or there can be hetererozygous variant. These are the ones who will be having such a high value of LDL. In terms of homozygous variant the most common cause is LDL receptor mutation. In terms of LDL receptor mutation, the only drugs which will work are MTP inhibitors that is lomit or there can be uh the newer angopoitin inhibitors.

[00:59:04]While for heterrozygus familial hyper cholesterolmia and all cases of homozygous hyper cholesterolmia which are not involving the LDL receptor you can start treatment with statin plus esetimi go on to PCSK9 inhibitor and if there is no response then you can go for the MTP inhibitor that is lomapite. So here the answer is definitely lomapite and if you look at the details heterroygus familial hyper cholesterolmia is common homozygus is uncommon LDL value more than 190 if it is more than 400 you should suspect homozygous as in our case there is poor response to drug therapy and that is why the management is tatin plusi followed by bcsk9 followed by mtp inhibition or angopotin inhibition inhibition that is via auma Now here while you are waiting for these drugs to work for immediate control of hyper cholesterolmia you need to use lipoprotein apherosis because when your LDL value is more than 400 statin acetimi PCSK9 inhibitors are unlikely to work. So you should shift the patient to upfront lipoprotein apherosis and then you need to try and put the patient on MTP inhibitors or AMGPL PTL3 inhibitors that is aumab. Unfortunately both lomapide and einumab are not available in India.

[01:00:33]So what you are left with in India is repeated sessions of lipoprotein apherosis.

[01:00:40]Now what is not the criteria for diagnosis of familiar hyper cholesterolmia? LDL of 130 is seen in a lot of individuals. So definitely that is the option you need to mark. LDL more than 190 and LDL more than 160 with family history is suggestive of familial hyper cholesterol. So if we look at the pediatric cutoffs uh there are different guidelines with different cutffs. So the Spanish guidelines suggest that if the LDL is greater than 190 at age less than 18 suspect that the patient is having familial hyper cholesterolmia. Uh if the LDL is more than 150 with family history of high cholesterol then still you should suspect that that patient is having familial hyper cholesterol. So both of our options they are being met.

[01:01:26]In terms of the European guidelines, what they suggest is that if the LDL is more than 190 or if the LDL is more than 160 with family history, then you should suspect that that patient is having familial hyper cholesterolmia. And what do the NICE guidelines suggest? If the LDL is more than 160, you should suspect that that patient is having familial hyper cholesterolmia. And what do the National Lipid Association guidelines mention? If the LDL is more than 160 again you should be suspecting familial hyper cholesterolmia. So anywhere what cutff is not given that is 130 130 is too low for familial hyper cholesterolmia. So that is the option you should be marking. Now a patient of mass with fifth four of 1.1 I think this we have already covered in our ADA guidelines. So if the fifth four is less than 1.3 you need to just repeat the fifth four one to two years. You need to put the patient on just diet plus lifestyle modification and no pharmacotherapy is required.

[01:02:29]If it is more than 1.3 then only you need to subject the patient to pharmarmacothotherapy. So here manage at periphery and follow every 1 to two years and just put the patient on diet plus lifestyle modification.

[01:02:46]Now what is the fastest increasing and most prevalent diabetic kidney disease?

[01:02:50]Again this is controversial. Most prevalent is definitely aluminuric decading. Uh fastest increasing with most prevalent will probably be aluminuric decad only but with increasing awareness fast is increasing with more screening which is happening and with urinary ACR which is now included in all guidelines for follow non-alic decade is also being picked up very frequently. So probably the answer would be most prevalent would be albinuric non-aluric would be fastest increasing because of more awareness but for this MCQ where both fastest increasing and most prevalent are mentioned I think the option you should choose would be aluminuric DKD. Now fineon what does it make it distinct from other mineralotic receptor antagonist? Does it have partial agonist activity? No, it is a pure antagonist. Does it cause irreversible mineralotic or receptor binding? Again, no. It causes reversible binding and because of this reversible binding, there is lesser risk of hypercalemia. Does it have tissue specific nuclear modifying effect? Yes, it causes recruit rec recruitment of core repressors and that that is how it has predominant action at the level of the heart and the kidney and that is why it is approved for use in CKD and it is approved for use of prevention of heart failure with u any patient with heart failure specifically heart failure with preserved ejection fraction does it decrease levels no it is a minocorticicoid receptor achamis so anytime you are blocking the receptor there will be falsely high aldoststerone values which will be there. So the option you need to mark is tissue specific nuclear modifying effect.

[01:04:39]A patient with diabetic keto acidosis what is the first step in management? I think this is an MC MBBS MCQ. Always IV fluid replacement first. After that check the potassium. If the potassium is low then give the patient potassium infusion. If the p potassium is normal or high then start the patient on insulin infusion. bicarbonate only to be given if pH is very very low.

[01:05:06]So answer here is IV fluid replacement.

[01:05:09]Next, what is not true regarding insulinoma? Interoperative pancreatic USD is useful. Definitely it is useful.

[01:05:15]Uh 72-hour fast is reliable. It is the gold standard diagnostic test. And on 72-hour fast, you'll be finding elevated ceptide, insulin, and pro-inssulin with low beta hydroxybutrate. So these three options are correct. Associated with men usually seen above 20 years 40 years of age. This is absolutely false. In men it is generally seen in 20 to 40 years of age. If there is no men when it is seen above 40 years of age.

[01:05:45]So the correct option is option B. So how do you differentiate a menociated insulin from a sporadic insulin? So sporadic insulin generally they are seen solitary they are seen in an older age group and they can be uh present anywhere in the pancreas while men associated insulinoma they are seen in a younger age group between 20 to 40 years of age they are often multiple they are often multif focal and there is diffused pancreatic involvement so that is why for sporadic insulinoma just inucleation is often sufficient while for men associated insulinoma you need more extensive surgery and uh in some cases you need medical management also. Now in terms of gonads uh two questions on aromatus inhibitors aromatus inhibitor with suicidal inhibition actually letool and anasttool they do not have suicidal inhibition they are reversible enzyatic blocket exame and formystain they both have suicidal inhibition. So both should be the options both should be the correct answers. Examestin is used now forestin is no longer used. Examest is oral. Formestin is intravenous. So if of the two you have to choose maybe you can choose e xame but I think both the options are correct.

[01:07:06]Uh how do the aromatus inhibitors cause bone loss? Again both the options are correct. So in terms of aromatus inhibitors they cause estrogen deficiency and because of estrogen deficiency there will be activation of wrankle which will be causing conversion of a pre uh osteoclast to osteoclast and at the same time there will be reduction in osteoprotectine production which will cause reduced bone matrix proteins. So both are the mechanism of actions but the predominant mechanism is through the rankal pathway through which it will be causing osteoporosis. So if you have to choose one of the two by rankal stimulation is the correct option. Uh now then a few simple MCQs of CH. So which of the following is not seen in a patient with 11 beta hydroxil deficiency? Remember any CH with hypertension you have only two options that is 11 beta and 17 alpha. So systemic hypertension is seen with 11 beta because in 11 beta there is precursors which have mineralotic action. They'll be causing hypocalemia and they'll be also causing virilization because of increase in androgens. So what will not be seen is salt wasting and which are the CH without salt wasting. So both the CH with hypertension that is 11 beta and 17 alpha they do not have salt wasting and then uh from 21 hydroxilase that is the non-classic variant it does not have salt wasting. So what is not seen in a patient with 11 beta hydroxilis deficiency salt wasting. Most common type of CH definitely it is 21 alpha. So straightforward question in a patient with Turner syndrome having aotic root dilotation. What should be the management? So here remember that Turner syndrome they can have two cardiovascular manifestations. Number one is aotic root dilation and second is hypertension. For aotic root dilation, the drug of choice is beta blockers followed by endotensin receptor blockers. For hypertension, ARB with CCB are the drug of choice. So here there is aotic root dilotation which is mentioned. So the drug of choice is definitely beta blockers. Diuretics they will cause dehydration and they will cause tachicardia.

[01:09:36]So that is why they will not be used for aotic root dilation. So the only option you're left with is beta blockers. So aotic disease present you should use beta blockers plus minus ARB. Beta blocker should definitely be used. If there is no iotic disease only hypertension then you need to use ARBs plus minus CCBs or thyides and then you need to remember the cardiovascular risk as well that this has never been asked but I think what you need to remember at baseline is that if the age is more than 15 years at least every 5 to 10 years you need to monitor the patient and the highest risk involvement is if the patient has based valve if the patient has co-actation of Aota or if the patient is hypertension with high ASI or high Z score then you need to monitor the patient every 6 months to 1 years while less than 15 years of age the lowest monitoring you need to do is every 3 to 5 years while uh the most high-risisk cases with basedotic wall hypertension or coactation of AOTA with Z score which is above three you need to monitor it every 6 months to one year so here the answer is beta blockers Now a 13-year-old presenting with Turner syndrome having short stature planning to start GH therapy patients wish to treat both growth and pubertal delay what is the drug of choice highdose oral estrogen absolutely no rapid development of uterus and rapid closure of epi epifises this should not be used wait till 16 years for attaining height and start on puberty induction to avoid premature epifises closure again know there have been trials which have been done which have shown that low dose of estrogen does not cause premature closure of epifises and start with lowd dose estrogen or start with transdermal gel estrogen. Now here uh ideally of the two you should be choosing the transdermal estrogen variant because oral estrogen will cause upregulation of SOCS and this upregulation of SOCS will cause reduction in IGF-1 because of GH resistance.

[01:11:46]So the best option is definitely start with transdermal gel estrogen at low dose and titrate slowly because this will not be having any impact on your growth access. So if you look at the new turner syndrome guidelines also they suggest that transermal estrogen should be used wherever possible because it has good aspect at the level uh of the growth also it has a good safe. So these two options they both are close and if you look at the present guidelines all the guidelines suggest that trans ddermal has the lowest impact on your growth because it will not be going predominantly through the liver and upregulating the SOCS followed by that you may use lowd do estrogen and then gradually add progesterone but of these two options because this lowd do oral estrogen this is what they are asking this is definitely uh going to be causing some reduction in your IGF-1 and here they're specifically asking for both growth and pubertal delay so all the new guidelines they suggest that upfront drug of choice is definitely transdermal gel estrogen at low do and then titrate it slowly what is false about overtesticular DSD most common kotype is 46x XX that is true breast development and cyclical hematia may be present. Yes, because there is both presence of ovaries. So this can cause estrogen which can cause breast development and it can cause cyclical hematuria and increased risk of glonidoblastoma. Definitely yes. So this is the incorrect option testice and over are present separately in all cases because there that is mentioned in the name only there can be presence of over testice itself. So there can be four gonads testice ovaries or testes or street gonads all can be present in a patient with OTDS.

[01:13:52]So false is option number B. Now last we are looking at the miscellaneous section. Which of the following is most common association in a patient with menfi syndrome? So menfi syndrome is a newly entitled term for patients having max mutation. Most commonly uh fiochromosytomy seen followed by pituitary adinoma followed by paragangloma followed by parathyroid adenoma and then ganglio neuroma can also be seen. So new term for max mutation fiochromocytoma paragloma most common pitutary neuroendocrine tumor rarely parathyroid adinoma and ganglion neuroplastoma may be associated. So the tumor spectrum is predominantly fo followed by pituitary adinoma followed by paragangloma. So the answer which is correct here is definitely fiochromocytoma.

[01:14:51]And in terms of the other men, I think most are aware of men 1, men 2 a and men 2 b. For men 4 again you need to remember it is very similar to men 1 but the mutation is cdk n1b gene. Here hyperarathyroidism and pituitary tumors are seen along with pancreatic neuroendocrine tumors.

[01:15:15]For men 2B this is MTC with red 918 mutation. So in red 918 mutation that is the highest risk and anytime the red mutation analysis is suggestive of 918 mutation you need to immediately do calcetonin and immediately do prophylactic thyroid thyroidctomy at less than 1 years of age.

[01:15:42]Fiochromosytoma screening has to be done at 11 years of age. So here a 5-year-old with positive mutation for men 2B 918 mutation is seen with men 2B. So immediately do prophylactic thyroidctomy. We are already late in this patient.

[01:15:59]What is not seen with gitleman syndrome?

[01:16:01]So jitalman syndrome is similar to use of thiocy.

[01:16:06]So thioide loop loses calcium. Thioides preserve calcium. So that is why they're also used for treatment of hypercalceura. So with gitalman syndrome definitely hypercalceia is not seen. It is associated with hypomagnesmia, metabolic alkalossis and hypocalemia. So rest of all the options are correct. Jitalman syndrome is same as use of thyide duretic. Barter syndrome is same as use of loop diuretic and loop loses calcium and thide preserves calcium.

[01:16:43]So the correct option which you need to mark is hypercalceia. So overall what we can see in our discussion is that there were two new topics where a lot of questions were asked. I think that is lipid disorders and second is focytoma paragangloma and this pattern they had a lot of oneliners this time around but with INISS we generally expect that the next exam can still have a lot of case-based MCQs which may be present. So uh this was more of a neat kind of paper. I hope you guys understood all of these questions and anytime you have your next INSS always go through the last two years of the INSS record. Thank you very much.