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Thyroid and Cardiovascular Diseases

Jan 22 | 1:30 PM

An excess or deficiency of the thyroid hormones triggers numerous cardiovascular complications, from atrial and ventricular arrhythmias to heart failure. These complications increase the mortality and morbidity risk within a hyperthyroid and hypothyroid population, respectively. Let us hear from Dr. Ketan Mehta, a renowned cardio-pulmonologist and diabetologist, as he describes his clinical approach to overcome cardiovascular challenges arising from an imbalance of the thyroid hormone.

[Music] a very good evening to everyone and thanks for joining in on our saturday evening i'm dr naveed and i welcome you all on behalf of netflix um for its 150th talk today and thank you all for being a part of this uh journey with us and uh for this session uh thyroid and cardiovascular diseases uh we have with us this evening professor dr ketan k mehta uh he's a renowned consultant physician uh cardiopulmonologist and a dermatologist based in mumbai uh with an uh spanning over two decades and um some saucers got a lot of uh experience under his belt and a lot of good content and i hope you all learn a lot from sir today thank you thank you dr a very good evening to one and all at the onset let me congratulate netflix and entire team you know today being the 150th program and i am delighted and honored to share this platform on this 150th you know to getting a hun 1.5 turns is is definitely a big achievement and i must compliment netflix for it friends all of you have heard of netflix for so many years and now you have got another platform from a medical fraternity of netflix and i'm sure in a time to come you will really have to choose that you know when you have a leisure time whether to go for a netflix or a netflix and i'm sure a time will come where you will select oh let me go for a netflix where i will be definitely benefited much more than rather than going to a netflix so no dishing with the netflix viewers but this is just comments alright so friends what i am going to discuss today is a thyroid and cardiovascular disease i am sure all of you have been seeing cases of thyroid day in and day out whether we talk of hypothyroidism subclinical hypothyroidism hyperthyroidism subclinical hyperthyroidism autoimmune thyroiditis and so on and so forth but what i am going to draw the attention over here is the thyroid dysfunction has a role in cardiovascular disease because we are seeing cardiovascular disease again so rampantly day in and day out so what we are going to focus or highlight over here that is there a rule of thyroid and cardiovascular disease and what is the role and how it is interrelated and connected so this picture shows you that there are various ways in which the thyroid can be associated you know the hypothyroidism has been associated with hypertension diabetes dyslipidemia and cardiovascular disease so if you look at the metabolic syndrome per se the thyroid also though not a directly part of metabolic syndrome it has been linked with all these entities and we are going to see it so now first let's look at thyroid and hypertension we know hypertension which is such a common condition where we see that a large majority of our populations which has got a hypertension and this is not just recent you know if you really look at the first the data published data about it which is way back we are talking of 1931 in fact there was this paper which was published in endocrinology in uh 1931 about the high incidence of hypertension in toxic goiter and in mexidema so this was the paper which was written by thompson ital in 1931 and they had seen that there is a high incidence of hypertension in maxidema and from that time onward the hypothyroidism has been identified as a common form of secondary hypertension so now we are talking of almost 90 years back when it was diagnosed that yes we need to evaluate for thyroid for a patient where we are suspecting secondary hypertension and now we have realized that value so much in current practice so before that let's understand about the thyroid in the cardiovascular hemodynamics because thyroid has got a relation with the alteration in cardiovascular hemodynamics all of us know that thyroid hormones that is what we call as p3 and d4 which has a effect on the heart as well as in the peripheral vascular system now what does it do in this overall cardiovascular system the thyroid hormone can decrease the systemic vascular resistance can increase the resting heart rate it will cause increase in left ventricular contractility and it will affect the blood volume so if you look at there is a tremendous effect on cardiovascular hemodynamics due to this thyroid hormones which is there now i want you to focus on these slides you know which is a beautifully depicts the changes in cardiovascular hemodynamics due to the thyroid hormones and it has very beautifully shown this is a paper which was published in circulation in 2007 and what i want you to focus is how the two extremes of thyroid condition which causes alteration or changes so if you look at the tissue thermogenesis we know in hyperthyroidism there will be increase in thermogenesis whereas in hypothyroidism there will be a decreased thermogenesis now what will it do in terms of systemic vascular resistance in hyperthyroidism there will be a reduction in systemic vascular resistance whereas in hypothyroidism there would be increase in systemic vascular resistance so what will happen blood pressure yes it is going to get affected it is predominantly the diastolic blood pressure which gets affected so in hyperthyroidism there will be a fall in diastolic blood pressure whereas in hypothyroidism there will be an increase in diastolic fluctuation what will happen to afterload in hyperthyroidism there will be a fall in afterload whereas in hypothyroidism there will be increase increasing afterload as a result of which there would be alteration in cardiac chronotropy and inotropy and what will happen with hyperthyroidism there would be definitely the heart rate which will go up whereas in hypothyroidism the heart rate goes down what happens to cardiac output in hyperthyroidism the cardiac output increases whereas in hypothyroidism the cardiac output will decrease and all these changes can lead to changes in pulmonary pressure secondly the thermogenesis which has been affected at the tissue level can also affect the renin angiotensin aldosterone axis and what we call dry success which can have a impact on the cardiac output also so if you see it's a very complicated and complex puzzled hemodynamics so thyroid hormone if it goes either hypo or hyper can alter the cardiovascular hemodynamics to a large extent okay so now let's look at this diagrammatic depiction about what is the three major parameters where it affects the one i mentioned is the vascular resistance second would be the heart rate and the third will be the basal metabolic rate so when we talk of the vascular resistance the thyroid hormone which relaxes vascular smooth muscle cells and it reduces vascular resistance so that is the one basic mechanisms where it is affecting the vascular resistance okay now coming to heart rate the obviously the pacemaker related uh you know the genes which are regulated by thyroid hormones and obviously we know that heart rate which gets affected by alterations in the thyroid hormone thyroid hormone also increases the basal metabolic rate in every tissue and the hypo or hyper functioning of the thyroid gland will directly alter the basal metabolic rate so these are the three parameters which will get affected so now let's look at we know that thyroid hormone which causes alteration in cardiovascular hemodynamics so how does it has an impact on hypertension now it is interesting to know that the blood pressure gets affected in both the conditions that is hyper and hypothyroidism in hyperthyroidism there is a arterial stiffness which is increased and that will cause rise in systolic pressure and it will cause fall in diastolic pressure so there is a widened pulse pressure pulse pressure is the difference between systolic and diastolic blood pressure so in hyperthyroidism you have a wide pulse pressure which is now what happens in hypothyroidism so we have already seen and we are going to discuss that there would be endothelial dysfunction and impaired vascular smooth muscle relaxation leading to increase in systemic vascular resistance which leads to diastolic hypertension in 30 percent of patients so if you try to recollect you know all your patients of hypothyroidism one third of them will have increase in blood pressure which is there over here so now let's look at the statistics if we have to see in terms of hypothyroidism and hypertension we know that 20 to 40 percent of patients with hypothyroidism have hypertension as i already mentioned one third of them have a hypertension of which predominantly it is the diastolic hypertension so you have a diastolic hypertension in a patients of hypothyroidism which is more common than systolic hypertension and it is primarily due to increase in systemic vascular resistance now you must understand that you have a two hormones that is t3 and t4 and t pha may act as a direct vasodilator and therefore vascular tone may increase in its absence that is in hypothyroidism and blood pressure in these patients is less sensitive to variations in salt intake so usually we say you know salt restriction which will be beneficial but remember one thing if your patient is having hypertension which is secondary to hypothyroidism it is not going to be responsive with reduction in salt intake so that is a a differentiating point which you should keep it in mind over here so uh here i am showing the prevalence of hypothyroidism in hypertension in india now that's very interesting to note over here you know this is a cross-sectional observational study of adult population with an established newly diagnosed hypertension and the second subset who is a hypertension plus diabetes and what was again found over here that amongst the new hypothyroid cases that of overt hypothyroidism so here it's a very interesting point so you know if you detect a sub clinical hypothyroid patients the prevalence of them is much more common about hypertension and not only hypertension diabetes plus hypertension again in more in this population so if you see why it is so now i am sure those of you have done or asked psh level routinely you must have seen there is a large chunk of population who has got a sub clinical hypothyroidism and when that is there that means the prevalence of subclinical hypothyroidism is so common you are going to get a population of subclinical hypothyroidism is much more than people who have a overt hypothyroidism and that is why you are going to see that hypertension which is more common over in this population so now let's look at when we talked about sub clinical situation i want you to focus on sub clinical both hyperthyroidism and hypothyroidism so what is the effect on hypertension i already mentioned that in subclinical hypothyroidism again it is a diastolic hypertension which is there whereas if we talk about uh the subclinical hyperthyroidism there is a possibly of course there could be a increase in diastolic blood pressure or there could be a increase in systolic blood pressure and as we discussed there could be a increase in white pulse pressure so hypertension overall is common in both subclinical hypo and hyperthyroidism more so in subclinical hypothyroidism and if you see the 2017 all the guidelines you know whether we talk of american college of cardiology american heart association american society of hypertension or all the hypertensive societies you know the in their guidelines for the prevention detection evaluation and management of high blood pressure inhibits what do they recommend measurement of thyroid stimulating hormone that is tsh is a basic test to easily detect hypothyroidism and hyperthyroidism which are the two remediable causes of hypertension so it has become a basic norm you know how you get blood sugar checked for all your patients of hypertension how you check your lipid profile how you check creatinine level similarly it has become a mandatory so friends do ask for tsh level as a baseline in all your patients of hypertension and you will be surprised you know even the people may not have symptoms of either hypo or hyper and you may find them either in the crank or having a subclinical thyroid dysfunction also so summary of this first part is that we know that cardiovascular complications are important in thyroid disorders because of high frequency in clinical presentation because we know the prevalence is so high and hypertension is associated with thyroid dysfunction and mainly to increase mortality and morbidity risk so we should screen for thyroid in each and every patient of hypertension okay so if anybody has any comments or any suggestions or points or doubts we are ready to take up before we move on to the next section of it so let's move the second portion that is thyroid and cvd the another important aspect is dyslipidemia again we are seeing so commonly lipid abnormalities in our routine patients and it is very important that you know lipid abnormalities have been implicated as one of the most obvious cause of associated cardiovascular disease we know that you know whether we talk of uh coronary heart disease or what cause of all cause mortality these are all seen in hypothyroidism because of one simple factor that it has been having an impact on the the coronary events also now there has been elevation in the certain inflammatory markers like crp and plasma asymmetric methyl arginine and platelet aggregating factor there are so many factors we cannot discuss on that this may contribute to the development of lipid abnormalities so these are all abnormalities which has been found with hypothyroidism now if you look at the biochemistry i'm sure you you may feel rebar pre vapours bio chemistry what the first mbps so i am not going to bore you with biochemistry over here but what i what i want you to understand that thyroid hormone has got an effect on lipid metabolism now what is the effect i mean it has been shown over here if you just broadly understand that thyroid hormone increases ldl receptor expressions okay it also increases ctp concentration and hepatic lipase concentrations so thyroid hormones that is t3 and t4 increases hepatic cholesterol synthesis by inducing hmg coenzyme reductase and decreases intestinal cholesterol absorption so the moment you have this thyroid hormone deficiency what is going to happen it will have a effect opposite to this and that will cause increase in cholesterol levels and that is how you get hypercholesterolemia okay so we know that there are various cardiovascular risk which are associated with hypothyroidism and what are those risk one is atherogenic lipid profile so abnormal lipid profile which is there abnormal hemodynamics we just discussed earlier there is a hemodynamics which are entered so one side you have got abnormal lipids on the other side you have got abnormal hemodynamics on the third front you have an impaired endothelial function you have a hypercoagulable state and then if there is a associated non traditional risk factor somebody has increased lipoprotein literally or some or increased homocysteine level or increase in crp level so all put together what is happening this hypothyroidism because of all these factors is causing an increased risk of a cardiovascular events now this table it's beautifully showing the lipid effects of thyroid dysfunctions so if you compare it hyperthyroid overt hypothyroid means there is a frank hypothyroid versus subclinical hypothyroidism now what happens the total cholesterol decreases in hyperthyroidism i'm not sure how many of you done this observation if you find a person of hyperthyroid and if you get a lipid profile then you will see there is a fall in total cholesterol whereas in hypothyroidism it is increased so obviously ldl is going to follow the same pattern so in hyperthyroid there is a decrease in ldl cholesterol whereas in hypothyroid it is increased now once the total cholesterol decrease even the hdl cholesterol also decreases in hypothyroidism whereas in hypothyroidism there may not be a front change which would be observed now triglycerides which are increase it can remain normal or slightly increase in hypothyroidism which is not change in hyperthyroidism and lipoprotein little a can increase in frank hypothyroidism and it can decrease in hyperthyroidism without any change in subclinical hypothyroidism now homocysteine there it came in a big way as a marker you know that hyper homocystinemia which is associated with a marker of atherosclerosis now let's look at what is the association between plasma homocysteine status and hypothyroidism and this is basically one meta-analysis which is shown over here and in fact i'm not i i think my data which is missing over here so what it is shown that in hypothyroidism there has been a significant or linear correlation of homocysteine level and this homocysteine starts coming down in a patient of hypothyroidism just by treating thyroid hormone so you are not giving a methylcobalamin or folic acid or you are not bringing down but just by correction of hypothyroidism you will see that there is a reduction of plasma hormone system levels now you are aware about this international classification of diseases which is there in most of the literature box wise and of which there are certain conditions where they are recommending that you must screen for thyroid dysfunction and which are there which has been highlighted in the box somebody who has a atrial fibrillation somebody who has a hypertension somebody who has a hypercholesterolemia or mixed hyperlipidemia that means we are talking of hypercholesterolemia as well as hyper triglyceridemia and diabetes you must screen for a thyroid level in this patients also so now as i mentioned the subclinical hypothyroidism which is a much more common entity than what hypothyroidism and what is the influence of treatment in comorbidities that is we are going to see now before that let's understand clearly about the sub clinical hypothyroidism now by definition it is very important that somebody who has got a persistently elevated tsh level persistently means we talk about more than three months so 12 weeks or longer elevated tsh levels more than 4.5 milli international units per liter that is what we are looking at so if you get a one single reading of tsh which is 4.9 don't just label him at a subclinical hypothyroidism so you need to see a three months apart that there is a increase in tsh level okay now that is your check for the tsh what about the other parameters that is normal total or free serum t4 or t3 levels you may check it repeatedly but it has to be a documented elevated tsh with normal t3 and t4 whether it is total or whether it is free and there will be few or no signs and symptoms of hypothyroidism you are well versed with symptoms of hypothyroidism that there would be increase in weight gain there would be a bradycardia there will be fatigue lethargic irregular menses so all these presentations which will be absent we are talking about that person does not have a clinical manifestation only biochemically and that is also the tsh which is elevated persistently beyond three months so that is one point which you will have to keep it in mind so now once you found or label somebody as a subclinical hypothyroidism they can be divided into two categories okay those who have a mildly elevated tsh that means the tsh levels is between 4.5 to 10 millia per liter and second category who has got a markedly elevated techniques beyond 10 million it could be 10 12 15 20 30 40 50. you know how much you can get the tsh you can get it in three figures so we have seen i'm sure quite a few of you might have seen the ts is going into 112 150 so that is also seen over there so here you house this situation where either it is mildly elevated or it is markedly elevated now if you talk about real incidents now there are various indian data which has been there about the epidemiology of subclinical hypothyroidism in india and look at the numbers you will be amazed that when we look at the general population you know this is various data from various studies by done by dr unikrishnan dr marwa dr roy little dr abraham it is almost to the tune of 10 that means 1 out of ten individual taken empirically we found to have a subclinical hypothyroidism and that is the large number we are talking about so that you should be aware that how much rampant it is okay now coming to this primary hypothyroidism and the severity of it and you know you must understand that why we talk about the tsh because if you look at this bar two bars like a straight line that is the normal range of tsh d3 and d now whenever the abnormality happens that is hypothyroidism the tsh is the first one to get elevated so that is the first abnormality in a mild disease it is the tsh which will start becoming abnormal which we followed by fall that is the decline in e4 and the t3 is the last one so in mild what will happen only tsh will be elevated in moderate hypothyroidism along with elevated tsh there will be a drop in e4 but t3 can still be normal and once you get a t3 which is low that means it is definitely a severe hypothyroidism so this is you must keep it in mind over here now why did i mention when i talked to you that you must document that there is an elevated psh twice three months apart before labeling as a sub clinical hypothyroidism because there could be a transient increase in tsh level and that is not putting somebody into a definition of subclinical hypothyroidism so what are the causes of elevated thyrotropin levels which are not related to thyroid failure or which are not related to hypothyroidism so there are various causes you know there could be a non-thyroidal illness and somebody who is recovering from it it can have this transient elevation of tsh then the recovery phase from any thyroiditis you know following a viral infection somebody can get thyroiditis and then there could be a transient elevation of tsh then there are certain drugs which can cause this transient elevation of tsh drugs like amiodarone lithium which is used in depression can also cause this then there is a lack of adherence to treatment somebody who has been put on treatment not taking medications regularly again there could be a transient rise in psh so we must take into consideration all these factors before we go for putting a label of somebody that he has he or she has got a sub clinical hypothesis now why we are talking so much about the sub clinical hypothyroidism what are the consequences so subclinical hypothyroidism it has been said that you know there will be a population who will progress into overt hypothyroidism remember one thing it is not that each and every individual of subclinical hypothyroidism will progress but there is a chunk of population which will progress to overt hypothyroidism so they will they develop the symptoms of hypothyroidism and they can have a become a surrogate marker for cardiovascular risk because of various factors which we discuss about because of dyslipidemia there could be a increased carotid intima media thickness there would be affection of the cardiac function so there would be a risk of coronary heart disease and congestive heart failure which can happen over there and that is why we want to be a definitely taking a preventive role for it so what is the rate of progression to over hypothyroidism in various studies it has been approximately three to 18 percent of affected patients per year so every year on an average anywhere between three percent to 18 percent will get become from sub clinical hypothyroid into overt hypothyroidism now this is a very interesting one study which evaluated the natural history of mild thyroid failure or what we call as a clinical hypothyroidism in 154 female patients over 10 year period and what was found over there that 57 percent of patients continued to have a mild thyroid period so that was a large majority of patients one third of them progressed to overt hypothyroidism and in fact nine percent of them reverted to even a normal tsh level so that also can happen so this just for your knowledge you should be keeping in mind now other aspect about dyslipidemia and subclinical hypothyroidism i was just mentioning about that why we are bothered about it because the lipid abnormalities which are implicated as a most obvious cause of associated cardiovascular disease coronary heart disease and all cause mortality in such clinical hypothyroidism so even this subset of subclinical hypothyroidism without even getting manifested as a overt hypothyroidism they are at a risk of cardiovascular disease because of they can have a lipid abnormality they can also have elevated markers of inflammation like a c reactive protein platelet aggregating factor and plasma asymmetric type arginine which can contribute also to lipid abnormalities so these inflammatory markers which can be attributed at atherosclerosis as well as they can lead to lipid abnormalities and lipid abnormalities i have already discussed with you which are the lipid abnormalities which are there so how do you manage this dyslipidemia in a hypothyroid patients so what would be would you be treating them with statins or would you be treating the hypothyroid so it is a standard dictum that all patients with dyslipidemia and overt hypothyroidism should be treated with limo thyroxine okay so there is no question don't be in a rush to start the statins because this dyslipidemia would be secondary to hypothyroidism and you will see quite a large number of patients who just by treating their thyroid the lipids will come down okay so that is one thing now obviously you will be monitoring with the tsh values and once the tsh values have normalized after two to four months of adequate levothyroxine therapy then you check the lipid serum levels and you will see that up to 30 to 50 percent decrease in the ratio of total cholesterol to hdl can be expected with levothyroxine treatment and that's the huge number which we are looking now if at that point of time if dyslipidemia has not been corrected then of course you need to know that yes my patient has got dyslipidemia which is not just because of the thyroid and i need to have other measures obviously therapeutic lifestyle changes and if required lipid lowering medications whatever appropriate most of them will require statins at that point of time okay now let's talk about the risk i was just mentioning cardiovascular risk in sub clinical hypothyroidism [Music] so the most consistent cardiac abnormality reported in these patients of subclinical hypothyroidism is impaired left ventricular diastolic function i'm sure you have seen so often 2d echo reports which mentions as lv diastolic dysfunction and you start wondering what is the implication now either these patients have uncontrolled hypertension or they have uncontrolled diabetes or they have uncontrolled thyroid status so just keep it in mind so if you accidentally happen to see a echo report which mentions lv diastolic dysfunction and you wonder from where this gentleman or lady got a diabetic diastolic dysfunction his sugars are controlled his bp is controlled or he doesn't have a sugar or he doesn't have a blood pressure issue check for thyroid level and if he has a subclinical hypothyroidism it can definitely be a cause for a diastolic dysfunction and it is characterized by slow myocardial relaxation and impaired ventricular feeling and it can result into of course which finally the heart failure which can happen so which you have to keep it in mind now we serve is let's look at the other parameters you know sub clinical hypothyroidism is associated with adverse prognosis in heart failure patients so if you have somebody who has a heart failure and if you detect that there is a associated subclinical hypothyroidism look at the difference you know you can see from this two diagram which is beautifully shown the cardiac event rate is better off or much less in a eu thyroid patient compared to sub clinical hypothyroidism and even all cause mortality you know even if you take care of other parameters the all cause mortality is higher in a patient of subclinical hypothyroidism compared to eu thyroidism so again it shows the importance of detecting that now this is a again a beautiful meta-analysis about the sub clinical hypothyroidism and the risk of coronary heart disease and mortality and it shows clearly there is a increased risk of cardiovascular events in all the studies of sub clinical hypothyroidism not only that it also has shown that with subset of sub clinical hypothyroidism there is increased risk of cardiovascular mortality so we are talking about increase in morbidity as well as increasing mortality due to coronary heart disease now it is not just that look at this bar diagram so if you understand the meta analysis interpretation over here from various studies even if you don't understand what i want you to focus over here that there is a increase hypothyroidism related mortality and that is what not just cardiovascular mortality but it is showing all cause mortality in subclinical hypothyroidism is increased so it is not just death related to cardiovascular events non-cardiovascular even deaths are also higher in a subset of patients with subclinical hypothyroidism so this is again a beautiful paper which shows that leo thyroxine treatment of subclinical hypothyroidism fatal and non-fatal cardiovascular events and mortality this was from united kingdom general practitioners research database and it has shown the outcome wise what is the difference over here and look at the numbers if you see over here if you see fatal and non-fatal vascular events in those subsets so we are talking of patients of subclinical hypothyroidism in the age group of 40 to 70 years if you see treatment whereas green line which received the levothyroxine treatment and look at the difference it's a huge difference so if you see the fatal and non-fatal vascular events there is a difference if you treat it versus if you don't treat it now if you look at the all-cause mortality yes it is definitely which has been much better off in a people who have been treated with it and not only in 40 to 70 years look at those in a senior citizen groups are about 70 years the two groups where treatment was given versus treatment not received there is a difference also which has been seen over there in both the groups also here so ladies and gentlemen what i want you to understand the continuum of dyslipidemia thyroid disorder and cardiovascular risk it is a continuity of it and this is my summarizing slide which shows that somebody who has got a subclinical or overt hypothyroidism which can predispose to dyslipidemia hypertension hemostatic abnormalities and if there is a add-on in children resistance like metabolic syndrome features then there is a multiple risk factors for cardiovascular disease which can lead to endothelial dysfunctions various cardiac alterations and then above which if the obesity adds onto it it is going to give rise to complete cycles and they are going to be at a higher risk for cardiovascular diseases so ladies and gentlemen please please do not take thyroid dysfunction lightly because this can definitely can lead to a problems from your perspective and can lead to cardiovascular dysfunction thank you so much for your efficient hearing and we would be happy to take up the question somebody wants to come on the stage someone to stay from the audience we would be happy to take up the questions for that hello hello good evening doctor yeah good good evening yes uh sir uh you have told that in case of a subclinical hypothyroidism if it happens more than 12 weeks yes if it is elevated elevated more than 12 weeks so i am a journal practitioner in case the patient comes to us we see hi uh sub clinical hypothyroidism and then we call him after six months so we should get the thyroid profile repeat repeat after 12 weeks yes absolutely normally if you see subclinical which we send the patient and say everything is fine income after six months yeah so it uh it would depend again that in what level you have got a tsh values if your tsh values are very high yes definitely you would call the patient earlier if the patient has got a tsh value is just a borderline you can definitely can wait for six months and can recheck it at the end of six months so that you will have to take a call individually if you find no here i am expecting that abnormalities then depending on that you can recheck it after 12 weeks or three months and then take a call for it so normally around 10 if i find psh around 10 and t3 t4 normal so i call after 6 months is the 10 correct no so then i would i would suggest you should recheck it at the three months rather than waiting for six months it would be worthwhile because you can pick up them early and then if required you can start the treatment at that point of time okay and should we go for free t3 t4 or a normal thyroid profile okay so if you are doing from a screening point of view then even at the sh and t4 be it free or be total is good enough you don't have to even ask for a complete profile of p3 t4 because as we have said that t3 is the last one to rise so even one single abnormality so if you get a t4 which is abnormal that is good enough so for the first screening purpose you can get t4 v8 either total t4 or a free t4 that is fine enough along with the tsh levels okay so what are the things where we go for free t3 because i heard in many of the conferences in ima they always insist that the journal practitioners don't go for free three t3 which is wrong no so now again it is a very uh important point so when if you get at the end of uh three months your tsh which is still divided which is elevated anywhere between 4.5 to 10 okay now your t4 which is normal and you are clinically suspecting there is a hypothyroidism so now there is a dilemma so clinically yes you are suspecting p4 which is normal and tsh which is between 4.5 to 10 now in such situation it would be advisable to get a free default because your total t4 may be normal but when you get a free t4 in such situation it could be on a lower side and this patient justifies for starting so it is a definite niche area so or else if you don't want to be little sure short before and rather than asking total people then go for only free t4 and because that will give you because the free t4 is the one thing which will be available for the body for its metabolism and effect so that is how you will check that level thank you okay thank you so much sir very amazing session it was very very clearly explained thank you so much thank you pleasure thank you dr puja for coming up uh dr ajay you can go ahead with your question hello yes good evening good evening uh sir uh is there any difference in rock salt and the normal iodine salt in the hypothyroidism present and plus the your advice in the regarding food we should be avoiding the hypothermia okay i i i'm so happy uh you came out with this questions so first of all the you know in good old times we had there was no government norms about the iodized salt now it is all the salt preparations which are commercially available which are coming as a hydra soil because otherwise there was in good old times there was in good endemic areas there was a huge goiter because of iodine deficiency now that part has been taken care of and it is all salts are iodized so we don't see at least in our country that iodine deficiency state and the goiter which was prevalent years back which is not there so that is one aspect you said but yeah yeah tell me but sir nowadays the peoples are more curious about the raw salt yeah rock solid organic salt mean to say they are so so even even those rock salts so they are have been because the commercially available preparations have been iodized so they are still definitely their sodium content is variable but the iodine content is still adequate so that is not an issue on that okay now coming to your second question which i like like anything the best part was you said about the food yeah and you know a lot of people will come and say that our neighbor has told this and that you can't eat green leaves yes now when you are taking any thyroid preparations the green leafy vegetables has got a competitive inhibition for the absorption of the thyroid preparations that means somebody who is having the green leafy vegetables and if they are taking the thyroid together it will hamper the absorption now this issue was more pertinent to western population who used to take even in the breakfast they used to take a green leafy vegetables because the salads and all they were eating the primarily this as a main food supplement whereas let's talk about the indian population how many of our population are having green leafy vegetables in their breakfast i would put it not even one percent let's put it all of us are either going to have it in lunch or dinner so by all practical means we should there should be a gap of four to six hours between having the thyroid preparations and green leafy vegetables so even that four hours i'm sure between the dinner he had on the preview she had on the previous evening and taking a thyroid medication is going to be four to six hours or even if we have it in lunch it is going to be still four to six hours between that so there would be definitely no restrictions i am making it clear no restrictions for our thing so it is only in the western world where they are having green leafy vegetables in the breakfast it is a matter so somebody specifically taking only green leafy vegetables all throughout the day then you will tell them not to have it in breakfast when they are having on the morning thank you okay answer uh what's the best time to take the tablet so it should be in the morning on empty stomach now again since you brought out this issue i i will give you an example i had couple of my patients you know the two incidences which i would like to mention it over here one patient he said since one week he was not taking the tablet and i asked why he was not taking he said my doctorate return it before breakfast and i was keeping my breakfast so i did not take the thyroid medication now see the logic no this has happened and i said yes now that is very important there is a difference what instruction we write so before breakfast is not equivalent to on empty stomach so empty stomach means they need not even have breakfast but still they can have so that is what it is important and the second point i want to say i had one patient who was taking one empty stomach is in spite of taking 150 micrograms of supplement his levels were not achieved and then going into history he said yes i am taking you and my doctor had mentioned it on empty stomach i am taking on empty stomach and i have cup of a large cup of tea after five minutes only so it is very important that what we say that you have it on empty stomach but nothing to be consumed for next half an hour so that is the most important part so this was the two real incidences i just wanted to share thank you okay thank you thank you sir thank you so much it's nice to meet you thank you thank you so much uh i was like request and you're on stage you can go ahead and ask your question so good evening sir so thanks for this wonderful presentation sir i wanted to have uh i have a query regarding subclinical hypothyroidism when at first clinical presentation patient has dsh of less than 10 but well in the subclinical range along with lipids along with pg which is well above 1.5 times uh the normal range so how would you treat it i mean patient is already bringing both these reports dsh as well as lipids are high so would you like to treat with thyroid state you need to understand that you know now whether he has a hypertriglyceridemia which is a dyslipidemia which is secondary to subclinical hypothyroidism versus his all endogenous hypertrophies and that we don't know right so here i would also suggest is first you wait repeat the tsh after three months and you take a call if at three months if his tsh is still elevated and you are already documented you don't have to repeat that radius right at that point of time you can might as well will start with the low dose of thyroid supplementation rather than correcting the disease but at the end of three months if you see his tsh is normal then you need to take a call whether you need to treat his hypertriglyceridines thank you thank you thank you thank you thank you so much for coming up uh we have dr pratyusha i'm accepting a request you can uh turn on your audio and video if you want um till then so we had a few questions that came up early and i've written them down here um so um what is the screening to prevent cbd and female uh familial uh hypothyroidism was one of the questions okay so obviously we need to check for the lipid levels get the cardiac evaluation done which can be done by ecg and if required even by a stress test to see whether they have got an underlying coronary heart disease so that needs to be screened definitely at regular increments so good evening sir [Music] so i have this case actually it's my case itself so the thing is about in 2019 i had a hypothyroid state okay along with lesser t3 t4 and higher levels of psh and i was started on 12.5 mcg thyron and i think i took it for about three four months and after which i started getting palpitations and a lot of restlessness whenever i took the medication so i had to stop it uh in order to you know at least stay calm and cut to the last year 2021 uh when i got tested uh everything was normal but the psh levels were slightly raised so i got the tpo antibodies done which were normal actually with a normal image so and also there is a hyperlipidemia okay and triglycerides and ldl levels are high so how do we proceed from this i mean what is the next step that i can take in order to you know control this okay so now if your uh t3 and t4 are normal if your thyroid antibodies are negative and tsh is less than 10 then probably you will not require any replacement for the thyroids hormone point of view because you know the very fact that you already started getting symptomatic so that means it was like over correction of your thyroid level so from you thyroid state you started going into hyperthyroid and that is what we want to avoid it so probably you may not require one thyroid second about talking about dyslipidemia we know that it is not that only the thyroid people will have dyslipidemia you can have dyslipidemia which is independent of your thyroid issue so that is what you need to be taking care of because this lipidima per se itself is so commonly prevalent so that is what uh we know about it so if required that needs correction but not from the thyroid thank you okay thank you so much so it was a great session thank you dr pradisha for coming in uh dr nadisha i've also accepted your request yeah go ahead dr father with your questions good evening sir uh i have a sir i'm having a hypothyroidism since three years and i'm taking medicines and the psh level is 32 now like but i don't have any symptoms and anything so should i continue this things or not yeah yeah you cannot stop it if tsh is 32 you need to bring it down so there is no question you will have to target it where you get a tsh levels below three so you need to step up the dose don't don't ignore it don't be happy so from whatever we can do it but it has to come up uh at the gradual intervals and you need to bring it down so don't get satisfied with whatever 32 levels we call it an end here and thank you so much sir for coming up to netflix and we hope to plan more sessions with you it was very interactive and we hope to see you thank you so much and i really enjoyed it and they use it and i i'm sure this is in competition with netflix thank you

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Dr. Ketan Mehta

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Dr. Rohan Desai

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