Blog

Introduction
i’m sandhya bihani and i’m 57 years old i’m mother of two a daughter and a son january of 2019 is when i was diagnosed with breast cancer i had my surgery a lumpectomy i also went through chemo after that i had my radiation and now i’m going through my herceptin infusion which will be for at least a year i was a person who was very reluctant on having my mammograms my ob gy would say oh annual mammograms routine i have no history of breast cancer in my family and i said okay before i go see my ob gy i’m going to have my mammogram done i went for my mammogram and then my routine mammogram test they found it and then they recommended biopsy and that’s how they found it it was stage one her2 positive breast cancer breast cancer

Finding Community and Guidance at Mayo
this journey and all that’s uh mayo has to offer the coffee and conversation the one that susan kane organizes for breast cancer patient which is once a month at mayo clinic to me that is very important because there are subjects or in information that’s shared during those conversation is very relevant to what i’m going through as a cancer patient there are a lot of experts or doctors or care providers who come and speak or share their knowledge and experience is something that i’m looking firsthand so instead of going and buying a book or trying to read online and not knowing i’m if i’m getting the correct information coming here once a month being with others who are going through similar breast cancer or other cancer treatment like i am being surrounded by them and sharing our experience laughing talking along with a cup of coffee and at the same time getting all the information that is pertinent to my treatment or something i may have missed i may have not even known all that information that they provide is vital and i look forward every month coming and being part of this coffee with conversation

Attitude with Gratitude
my motto is attitude with gratitude if you have the right attitude and at the same time having gratitude for all the people everybody professionals your family friends who are helping you in this journey to appreciate them and be thankful for everything that you have the future looks so bright the future is awesome because i know i’m in the right place i’ve got the right treatment everything is falling in place so we look forward to seeing every stage in our life with a lot of love and enjoy every moment that we have

Vernice’s Story: Finding Peace Through Answers
my name is vernice grossglass i’m going to be 54 very shortly i am here because i was asked to talk about my journey with breast cancer i was diagnosed last april 2018 triple negative stage two when i discovered my own breast cancer i immediately mayo was the first name that popped in my head i feel like they are family because i’m here i was here all the time and you have a team of professionals and it seems like they just focused just on you and i know that there are other patients but it just felt like you know the attention was on me and let’s see what we can do to help her and i just they were just wonderful and i just felt like i knew i came to the right place and that they were going to help me eradicate my breast cancer then you know i thought okay this this can’t be happening to me not no why me and then i thought okay i don’t want to die i i have i have a lot to see i want to see my son get married i want to see my first grandchild and so i was scared because i didn’t have answers and once i got the answers from mayo then i was at peace with everything what was fixing to happen to me they gave me a plan of what they were planning on doing and i was like okay let’s do this

Support Systems and Shared Strength
i also have you know two other friends that also went through breast cancer at the same time i did and we all had the same type of breast cancer so i already had a support group and we would just talk and ask each other how we’re doing and what’s going on with your treatments and so i really do think that having other people you know talking with other people who’ve experienced the same thing as you just kind of makes you feel like okay i’m not alone this does happen to ordinary people and it just it is what it is but we’re you know we’re gonna survive we’re fighters so and i’m definitely a fighter and i’m feeling great now so talk with other people if you have fears because i think that talking is good therapy just and even if you’re talking to someone who’s never experienced it before it’s just good therapy to talk about it get it off your chest and and share your feelings of how you’re feeling and i going through it i also had my moments of depression i had meltdowns by myself you know feeling sorry for myself but like i said once i got the answers i felt at peace with everything and i knew that i had good people helping me which is dr mclaughlin doctor chelmsford dr rinker and all the nurses everybody they were just wonderful and so definitely talk you know just share your stories because that that’s good therapy right there um the other women that i encountered while being here we we would talk and they would with their experiences because they were like survivors and they would tell me what worked for them what didn’t work for them yeah just having answers that’s key to having answers because then you know what you’re dealing with and then just you work your life into that and just don’t let cancer stop you from doing the things that you enjoy doing you know and that’s life the rest is history but i feel great

Dave’s Story: A Call to Men
my name is dave wiggum i’m 60 years old and i’m a currently in treatment for breast cancer here at mayo i was in the shower one morning and felt a little something on the side of my nipple and so i mentioned it to my wife and she said you should talk to your doctor about that and i said oh you don’t have an appointment in a month i’ll talk to him then i remember when i first talked to my doctor about it he said well that’s probably nothing let’s get it looked at and so they did and finally the day came where they called me to tell me what the results of the biopsy were and they said actually david you do have cancer and so i was diagnosed with cancer in january of 2018 came and met with the team here at mayo and had surgery in february of 2018. you know i i don’t really have breast cancer in my family i was just the lucky one millionth customer i guess but that’s okay i never really focused on is this a male or a female disease it’s just a disease i have breasts and and there’s a there was cancer in them um so you know i would say it’s a it’s a a marathon it’s not a sprint don’t let it define you and you know keep your head up because where your mind leads your body and your your healing will follow

The Power of Support and Speaking Up
the other thing that i would tell people is and this is a big one i i tend to be very self-sufficient but you really want to have a support person come to those those those appointments with you because there were times my wife would say oh she said this and i wouldn’t have that in my notes just because there’s so much and so having a good support person to both be there for you but also attend those appointments is really helpful i’m a very private person and so i usually don’t talk with anyone about my my private experiences i just don’t and a lady who works with me i was on the phone and i got tired of running down the hall to a conference room to talk to the doctor so i just took the call right at my desk and afterwards this lady wore something camera and she said dave i didn’t mean to listen in on your conversation but i heard it and i just want you to know you don’t have to do this alone and i said well thanks i appreciate that and that really changed things for me because i decided to tell everybody i decided to not only not keep it private but be very vocal about it because i wanted men to learn that you need to do self-examinations you know it happens it happened to me i never self-examined myself i just got lucky but i would encourage men to to talk about it to be open about giving themselves exams do that to give yourself the best chance to find something that might be there you know there’s always bumps in the road for everybody and this is a little bump for me but i found it early and i had a great team of people who are helping me deal with it i never felt funny about having breast cancer but i feel really good about being someone who can spread the word that this happens to men too and so that you need to be doing things to keep yourself safe

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Introduction
hello viewers a very good morning Welcome to our FP live session and today our topic is what is blood cancer what are its causes symptoms and the latest treatment options available with us and today for our discussion we have with us Dr padmaja loii ma’am she is a consultant hemoncologist and bone marot transplant consultant at Apollo hospitals ju Hills Hyderabad and ma’am is also an expert in treating bone marrow transplant leukemia Myoma lymphoma enemia and low platelets so dear audience if at all you have any doubts related to blood cancer or any other diseases which I’ve mentioned just leave your doubts in the comment session and Dr paja ma will be taking them uh live during the session hello ma’am Welcome to our live session and so dear audience sorry and so dear audience uh just leave your doubts in the comment SE we going live now uh ma’am as our topic itself says what is blood cancer let’s so let’s start off with the first question please answer

What Is Blood Cancer?
so blood cancer is another ter called a leukemia so there is an unchecked mechanism where the abnormal cells are proliferating in the blood so what happens when you’ve got an excess of very immature blood cells which proliferate they take off the normal space for the normal cells that is why you get uh low blood counts like low hemoglobin low platelets but in turn white cell count will go very high that’s the time when we do a special test and the simple blood test like CBC will show a very high white silk count and under the microscope you would see a cells called Blast cells that’s the time we suspect a leukemia and do further test like bone marrow to confirm this there are various types of leukemias some could be coming on in very few weeks so the patient is very well and within the next 3 weeks they become very unwell and having a diagnosis of leukemia they are called acute leukemias they come on very sudden with a very short distance short time duration and chronic leukemias are indolent they go slowly and they they develop over a period of time months to years and there is no immediate life threat because of chronic leukemias they can be managed sometimes as an outpatient maybe a short inpatient state but acute leukemias where they come on in a short span of time in otherwise well patient are the ones which are life-threatening and have to be diagnosed in time to have a good outcomes

Causes and Risk Factors
ma’am what are the causes for this uh blood cancer what what is the reason behind of this starting or forming in the body that’s a a good question har every patient who comes through the door will ask this question why did they develop leukemia and they’ve not done anything wrong this is very true almost 95% of the times we don’t have a reason unlike liver cancers where you’ve got a history of alcohol unlike lung cancers where you have got a chronic history of smoking in blood cancers you hardly have any precipitating event which patient has done it they come as a denovo there is some mutation in the genetics which has happened and they change over to a leukemia and most of the times these are not hereditary they have not born with it they developed this genetic mutation in the couple of weeks prior to this diagnosis so there’s nothing they could have done to prevent it however there are few reasons what we say that they may enhance the development of leukemia like uh you know where there is uh radiation exposures this is main mainly so in areas where there is atomic bombing which we have seen and uh Benzene chemical dies people who work with a petroleum products uh in people who work in petrol bunks they should wear gloves all the time because they’re consuming these chemicals all throughout or excessive use of pesticides there also a certain culprit which can increase the chances but they do not de over cause the leukemia

White Blood Cells, Red Blood Cells, and Platelets
so ma’am as you have mentioned that increase in the white blood cells count is what results in blood cancer in the other way can we even say it as because of the red blood cell count is also low in these patients or the red blood cells remain high as well as the white blood cells count increases so the first thing is white cells are increasing when they start increasing there is no space in the bone marrow for the normal red cells and pl platelets so the normal cells are being replaced that’s why you lose the hemoglobin you lose the platelets so in the initial phases you may not have anemia and a low platelets you may just have a high white cell count to start with and as you go further you will develop the rest of the features

Differentiating From Dengue and Other Conditions
so how do we identify ma because one of our known family friends I’m just taking it as an example so even audience can connect to it they were having U sudden fatigue and having vomitings and after going to the doctor and after blood test and everything they in the local hospital they said it is denu fever after they going to a corporate hospital after some series of tests they said you have blood cancer so they were in a shock they said all the others were just saying dingu because of the low plateless how can you just say it is bone marrow because many people uh sorry blood cancer many people have these small small minor doubts because of low platelets because of no Red Blood so please bust these all these mths sure so when whenever we have an abnormality suppose the leukemias can just present with fever extreme tiredness or infection they had fever they had some antibiotics not settling that’s the time you go ahead and do a blood test blood test is a key important investigation and also looking at the blood under the microscope is another by an expert is another key thing whenever we say denu fever we need to have an establish dingu IGM or ns1 something positive so it’s a definitive evidence that you’ve got a dingu and it’s it’s not a presumed that it is possible dangu and second thing you look under the microscope and you should not have any abnormal cells if you do not have a definitive diagnosis you should always follow it up because Dango fever platelets will settle back to normal s about a week’s time and if they don’t settle or if you’re seeing any abnormal cells or you’re dropping your hemoglobin which is very unusual in denu or a highbid cell count so these are the things which raises suspicion and then further investigations will confirm so a key important thing is to have a definitive diagnosis and do not have a presumed thoughts about a denu and if things are not settling you should have further investigations and have a definitive cause for your problem

Which WBCs Increase?
ma’am we have a question from an audience uh he is a doctor and he says uh he’s asking which type of WBC is increasing okay so in blood cancers as we said there is an acute blood cancer and there is a chronic blood cancer if you’ve got a CBC done you would have a very high number of atypical lymphocytes that is generally in ALS you could have a lymphocytosis normally lymphocytes are about 40% and if you are having 80% of lymphocytes then one has to think that there is an abnormality or if you’re seeing myocytes or you’re seeing increase in number of atypical cells or a blast that’s the time you should suspect there is a acute leukemic process suppose if you’re seeing the neutrophils are high occasional nrpc then there is a some condition called a chronic myoid leukemia where the white cells are high patient is otherwise well initially they think it’s an infection but once we confirm that it’s persistent and there is a little bit of spleen we do a specific test called a BCR abl PCR and confirms the CML diagnosis so in a sense it’s more of a lymphocytes atypical cells blast cells any amount of abnormal myocytes which should not be there in the blood smears then you should suspect there is something going wrong with the blood disorders

What Are Blast Cells?
so ma’am as you are mentioning blast cells which is something a new term that we are hearing apart from the red blood cells white blood cells and plasma and the platelets please uh elaborate a bit about this blast cells so blast cell means it’s a very immature cell normally they should just reside in the bone marrow and they’re less than 5% in the bone marrow if they’re in excess in the bone marrow they come out into the bloodstream and you should not see any blast cells in the blood smear if you see even one you should start thinking there is something seriously wrong blast cell is nothing but a very immature large cell and you should not see it in the peripheral blood whatever the blood test we do we should not see that we start seeing it in the your report you should inform you should consult your hematologist

Staging and Related Blood Cancers
so ma’am in blood cancer are there any stages because sometimes doctors say have have come late because there were no symptoms you couldn’t identify it in time so are there any stages and so that we can come ahead and look look for treat so blood cancers in a generic term we are talking about a leukemia but in generic in general population a lymphoma Myoma these are the other bone marrow cancers they are also called blood cancers by many people so lymphoma the people can present with the lumps in the neck lumps in the axilla you know under the armpits that’s how people will know and another reason how people present with a lymphoma is ongoing fevers they have no reason they have continuous fevers this is called pyrexia of Unknown Origin and during the investigations people will have several tests including CD scans and they find some enlarged spleen enlarg lymph nodes and following that they would have a biopsy and will have a diagnosis of lymphoma but blood cancers most of the time they are in the blood so they are stage four so you don’t have to worry just because it’s stage four does not mean that it’s not curable many of the times in blood Related Disorders we do find them coming in stage four unlike lung cancers the stage four carries a poor prognosis but blood cancers do not carry such kind of a prognostic value depending on the staging but what is more important in blood cancers is how well you are when you presented and when we made a diagnosis if you’re very unwell you started an ICU your outcomes may not be good so early diagnosis is always the KE key for a better outcome and also blood cancers are very expensive diseases and we can cut down the cost of the treatment by 50% if you started as an outpatient rather than being very unwell and started in an intensive care

Life After Treatment and Remission
uh ma’am we have a question from an audience man if the blood reports are normal after chemo and radiotherapy will the patient return to normal life in future post the treatment so it is a very generic question it depends on what diagnosis we’re talking about is it a chronic my or leukemia is a is a diagnosis many people correlate where the blood cells are abnormal patient otherwise well and you had a BCR abl particular genetic mutation has happened and you keep monitoring that particular mutation and if that returns to normal you need to continue the tablets and people nearly have a normal lifespan but other blood disorders there is a lot of followup depending upon the stage of the disease how good the response to the treatment is what we call as how deep the response is with the chemotherapy the deeper the remission we call it as a complete remission or less deeper then you call it as a partial remission that response depends on the intensity the type of disease in particular patient you can assess whether they need a three monthly followup six monthly followup or they need a surveillence CT scans to see that is there any chance of disease coming back in generic we say for about 5 years after the treatment if you’re disease free you could be be considered as a Curative from that particular disease until that time you may need a very um distant followups but you do need to consult your consultant regularly perhaps it may be a three-monthly basis

Diagnostics: Tests and Technologies
thank you ma’am and what are the diagnostic measures to identify blood cancer so a simple blood test called a CBC is the first one which tells us there is a suspicion following that it may be a bone marrow aspiration and biopsy we do bone marrow aspiration and biopsies most of the times to know the prognosis rather than confirming the diagnosis and in that there are a lot of special tests we do a test called flow cytometry where you are actually knowing the markers on these cells previously many years ago about talking about 15 20 years back we didn’t have all these tests so we used to see the blast cells under the microscope there are large cells there are particular size and shape how they look and the expert will say this is acute my or leukemia the other one will say acute lymphoid there are times s you are in a confusion but now with a specific test like flow cytometry it’s very objective you have got a certain set of markers then you can say you know acute myoid or certain set of positivities then you can say lymphoid so it made things much easier more objective and you are able to detect at a very low level so you can monitor the treatment as well after you’ve responded with the treatment you can see how low even one cell abnormality among the 10,000 you can detect by means of these sophisticated test now so we know that the deeper the response after you give treatment the deeper the response the better the outcome is and there are specific test called the cytogenetics you look at all the you know 23 pairs of chromosomes to see which chromosome has got an abnormality to generate this leukemia and after the treatment you want to look back and see that it’s clear or you look at a genetic mutation on a particular chromosome there may be a gene which is amplifying and you want to measure that and see that is gone back so if you identify some problem before the treatment you want to monitor that after the treatment to see that it’s gone away so that’s the importance of doing these special tests to know the depth of the response

Treatment Options: Chemotherapy, Transfusions, and Procedures
thank you ma’am and coming to the treatment options for blood cancer could you please elaborate a bit because the moment we hear it is blood cancer many people think just blood transfusion uh might be the treatment but not something else and they are in search of various methods and mechanisms but many people lack of information is what is exact treatment for blood cancer which is the effective and the latest please elaborate so blood cancer the only treatment is chemotherapy generally surgery is not an option because blood is circulating everywhere so we cannot take them out from the cancer cells you cannot filter them out and radiation very rarely given that is part of the bone marrow transplant we do but all over the treatment for blood cancer is chemotherapy you cannot transfuse or filter the blood and remove the cancer cells uh many people do think that that is possible but it isn’t there is one procedure called leukopheresis when patients come with a blood cancer with a very high Whit cell count like two lakhs three lakhs and they’re compromised in the lung with oxygen that is the time we filter out these white cells and it’s a temporary process we filter them in order to give us a little bit of time that patient does not deteriorate and then we give chemotherapy so when we filter yes it can come down from 1 lakh to about 50,000 or 30,000 from the white cell count but if you don’t filter for 2 days it will go back to the same level so whatever the filtration techniques are very temporary just to give us a day of time for the chemotherapy to work and only these are done in an emergency situations in an intensive care just exchanging the blood or giving blood you can imagine blood cancer the billions of abnormal cells and the amount of blood blood we are giving is a very minute amount we have about 5 L of blood volume and when we give a blood transfusion you’re hardly giving about 300 ml so you cannot uh exchange the whole thing and there is a constant process blood cells are forming every day every hour so you cannot replace the abnormal cells by means of this so what if we do that you are just taking a drop out of the ocean this is what you do

Key Symptoms to Act On Quickly
ma’am we have a question from an audience and actually we have discussed this earlier by Dr DEA what is one common symptom which we need to observe in leukemia to react fast so leukemia yes low platelets where you have a bruises and bleeding or extreme anemia or very high white cell count on the blood test if you see a blood test with a white cell count more than 40,000 more than 30,000 immediately you should go and see hematologist within 24 hours because sometimes the blood cancers are progressive very fast so you do not want to waste time

Sharing Reports and Follow-up
thank you ma’am and one more patient who had earlier asked about the blood reports he’s requesting if we can send his reports through mail so that you can have a look at it and all sure definitely sir we will shortly once the session is done we’ll share you an email ID to which you can send your reports and we will get it verified with Dr pja ma’am and we’ll get back to you

Bone Marrow Transplant: Role and Outcomes
thank you and so ma’am when we are when you’re talking about this blood and all so as please correct me if I’m wrong the blood cells are generated in the bone marrow is what is commonly known please correct me if I’m wrong so if at all we do bone Maro transplant for the blood cancer patients uh will their survival rate and the recovery rate increase and will they lead a normal life like earlier so the question you asked me uh one simple answer is yes but it’s so complex you cannot just say the answer of yes there are multiple variables involved in so blood cancer yes definite Curative treatment is B transplant but not every blood cancer patient needs a transplant so primarily you have to give chemotherapy to get the disease into remission we use the word remission that means that cancer is not detectable by any means what we know it does not mean that it’s completely cured because there may be a small number of cells we cannot identify them by the current means of any of the testing as I said there are lot of sophisticated tests now we can detect one abnormal cell among among the 10,000 normal cells so that is our ability to test it anything below that we cannot identify and these SK cells can abnormal cells can remain dormant and can grow back again this is what we call as disease coming back or relapse in a patients with a leukemia we always think about what is the risk of this particular patient if they’ve had a good response good genetic then we think that his risk is very low so we don’t consider bone Mar transplant but suppose if they had some abnormal gen IC variation and we know those are associated with the increased risk of disease coming back or they’ve not gone into a good response how we were talking about you know the MD minimal residual diseases positive then these patients needs to go through a bone marrow transplant to prevent this disease coming back at that time we give intensive chemotherapies and sometimes we use a total body irradiation mechanism to clear out any dormant leukemia cells lying anywhere and also to give a new immune system from a new donor that is the donor immune system to fight these leukemia cells to keep a check on these new leukemia cells anything developing it just takes off from the immune system so this is the process of bone marrow transplant it has got a good cure rates provided the first remission if you do a transplant the outcomes are good the patient when he comes he should be in a fit position and have a good disease response and donor status as well makes a difference supp you have got a sibling donor the transplant is easier compared to unrelated compared to a hlo donor so there are multiple variables in it sometimes if the patient has got a very bad disease type we would want a little bit of graft versus host disease and we actually choose an unrelated donor superior to the sibling so there are lots of permutations and combinations in a given patient for what is good for them yeah

Transfusions During Treatment
thank you so much ma’am and ma’am uh in uh blood cancer patients when they regularly uh get their blood test done weekly or for every fourn night and all if at all their blood cells their red blood cells and the count drops in they the doctor suggest them to immediately get some blood transfused or platelets be given to them is it advisable and is it good that they take regularly uh these Bloods and all because taking blood and platelets from different different people is it a good thing to take and will that support them a lot uh that’s it’s a great question har so blood blood cancer treatments are very intense when you’re giving intensive treatment it literally takes off all the normal cells and an abnormal cells in the bone marrow in order to get a cure at that time your blood counts are going to drop down your platelets are going to go down you definitely need a transfusion otherwise we cannot survive with a very low blood count and it’s not going to we know that it’s not going to recover that quick so we need to support it there is no doubt that we need to support it there are different things we can do in order to reduce the risk so all the blood is tested for all the viruses like he B hepatitis C you know HIV in a very sophisticated manner what we call as a knack testing where you can detect it a very very low level so that makes it almost 99% safe and uh we give lucco depleted so we remove the white cells from the blood we no longer give whole blood so that practice is almost obsolete what you see in a movies like you collect one person’s blood and give it to the other person it is never never done after the 1970s that process has been stopped so we now what we call as a components the blood is separated into red cells and platelets so only the packed red cells what we give what we call is a blood transfusion so you only have the red cells even a tiny amount of white cells we remove it with what we call as a lucco depletion filter so there is a specific uh transfusion filter sets available you can remove those white cells by doing so by repeated blood transfusions you don’t get transfusion reactions there are certain things you can limit by doing that and platelets as well single donor platelets are always superior rather than a random platelets it is always good to have you know a donor who is male healthier who would be able to give a larger volume of platelets and we can actually rotate the same donor the donors can donate every week of platelets they will not lose any of the platelet volume in them blood you cannot donate for 3 months but platelets you could be a regular platelet donor as well for your loved ones if you’re supporting with their cancer treatment and the need a frequent platelet transfusions you could perhaps have four donors and then rotate them around to have the platelet support in that way you minimizing the amount of uh donor exposures so there are a lot of measures we take to prevent and one myth people say is can we have our relatives who come and donate blood no blood is always a replacement we do a lot of processing to prevent any of these reactions so feel free to discuss about these and the blood now is safe there are a lot of tests we do to make it safe and lucco depletion is one using a single donor and of course whenever we don’t need to give blood transfusions there are alternatives we should always go for that

Platelet Donation Explained
and ma’am uh I I have a bit knowledge about the platelets but please elaborate a bit about audience because recently my husband has donated his platelets and for the first time we are seeing that uh initially the blood was flowing out it was taking in platelets and again pushing back the entire blood which is uh for our surprise that oh we didn’t know know that only platelets will be taken and his blood will be given back so please explain a bit about the this is called a platelet donation what we were just talking about it’s a single donor platelet donation that means a donor comes only he’s donating platelets so it is similar to a dialysis machine it looks you put a needle one blood will flow from one arm to the machine the machine will filter out and only takes a platelet so you put a frequency where it has to filter and it will filter the top layer of the blood and the remaining red cells everything will be given back through the other arm into the same uh you know donor so they won’t lose any of the hemoglobin they’re only collecting the platelets and that’s hardly about 200 we collect and it depends on the patients you know the person who is donating their weight and height then we decide how much to take it people will not feel tired it just needs that you need uh two Pricks on both arms and about it takes about an hour to two hours for the feres to go on so there is no harm in donating this at all

Donation Frequency and Myths
thank you so much ma’am and dear audience as Dr padja mam is mentioning plates can be platelets can be donated once in every week and blood can be donated once in every every 3 months so uh it is benefit of the patients and your family members who all are in need of this blood and platelets please do please do go and donate and then there is I don’t know whether to call it as a myth or it is a fact uh people say that the more often we donate blood the more we get active we get new blood and and all all that stuff you might be knowing all that what you hear so please tell us a bit about that so people do feel that I think it’s a psychological impact that they feel happy that they’ve done something good and this is a voluntary people are not paid for so it just gives you a lot of positive impact and there are certain people who are polyamic that their hemoglobin is high because of smoking or whatever the reasons when you have a too much of blood it gives you a headache so those kind of people when they donate they feel they become a bit lighter they feel a bit refreshed that could be the reason but more so it is psychological they feel better about it

Costs and Financial Considerations
thank you so much m’ and one of the audience is asking uh Revenue part for the testings I think he what he meant is not Revenue I think he has asked for the cost for this test for the blood cancer test so I would like to mention Here My Dear audience that the test may be vary we cannot say exactly what could be because once the doctor sees and does your basic CBC test which Dr padja has just mentioned earlier so the regular test and the other test will be followed as for prescribed by the doctor so you can get in touch with your doctor doctors at your own centers and get to know about more information and if I think uh there is a little bit of a difference what you’re asking it’s a simple CBC will cost about 200 to 300 rupees but that’s very simple where you suspect and a bone marrow just if you’re doing a bone Mar aspirate and biopsy it will cost you about 10,000 and that all again the cost will differ along whether you’re using disposable needles whether you’re using a reusable needles whether you needed a sedation to do a bone marrow how comfortable you wanted your procedure to be and how sophisticated test you want you can make a diagnosis of leukemia without any of those sophisticated tests you don’t need to have a flow cytometry you don’t need to have a fish but all these extra tests are giving you a little bit more information but by all means you can diagnose leukemia by simple bone marrow test and a basic test which would be cheaper but there are lot of things that available now in the market internationally so we call it as a FL cytometry fish and the new test has come called the Next Generation sequencing that will cost quite high but it only gives one additional information it may or may not be that useful if you’re somebody who have enough money you could have it but you don’t have to have all these tests to have a Leukemia treatment so feel free to discuss with your doctor what are your financial constraints and what is the absolute minimum you need to do for the testing and what is the extra thing what benefit you get so always feel free to be open to discuss these things because now we are Global Market we have got everything available what is new in the market the newer things are always going to be expensive but they give a little additional information that may not be necessary for every patient so feel free to discuss with your doctor about the need for these new tests

Immunotherapy and Emerging Treatments
uh ma’am we have one more question ma’am is immunotherapy suitable for blood cancer so as per se immunotherapy is not generally part of blood cancer treatment specifically in acute lymp blastic leukemias there is cd20 positive so some patients we give a rxm up along with the chemotherapy and generally immunotherapy is not part of the Leukemia treatment there are few new molecules are coming they’re still in the trial process

Blood Cancer Care During COVID
thank you ma’am and as this is now we are in this pandemic of everybody is in the scare of covid so what is that the blood cancer patients need to take precautions so that they don’t get this infection and if at all they delay the treatments what would be the adverse effects so one thing is the common thing what we are seeing now is the delay in diagnosis because of the scare of covid people are coming quite late for confirmation of diagnosis they come through most of the time through emergency and then we confirm leukemia or the most of the covid symptoms are very similar to leukemia they’ve got fever they’ve got shortness of breath and they’ve become anemic so these are the three key things the simple thing early diagnosis is by blood test early blood test CBC any abnormality consult as an outpatient you could do the covid testing beforehand as an outpatient during the treatment somebody has got a positive leukemia they don’t have to worry about covid because leukemia is more life-threatening than the covid so continue your treatments and if we look at all our leukemia patients they’ve not had a higher incidence of covid and we’ve not had patients who have lost U during the leukemia treatment because of the covid most of our patients are well known to take all the precautions what we talk about wearing the mask and taking the precautions and yet another thing a follow-ups is very important people stop treatments and it’s actually the disease coming back which is killing the patients rather than the covid so be aware of these life-threatening conditions and find out alternative Avenues where you can reach out to your doctor it could be uh telephone consults and doing a regular checkups keeping in connection with your doctor if not physically uh from remote and continuing your treatments perhaps you can discuss and reduce your intensity of treatments for a time period but do not stop following up so it’s very important to continue treatment

Services at Apollo Cancer Institute Hyderabad
thank you so much ma’am and please tell audience about the blood cancer treatment available at Apollo Cancer Institute Hyderabad so blood cancer one we believe it has to be very much integrated you need a lot of support from the laboratory from the blood bank intensive care along with a specialist on board and it’s a teamw work and we want to have all the systems in place and Under One Roof so the tests and the procedures are very quick if you had come with a suspected leukemia within 48 Hours within 24 hours you need to confirm your diagnosis you need to get on with your treatment we do not have time to wait for too long so all these processes are available to have a quicker diagnostic modalities inh house and to start the treatment early and if you needed a transplant the same processes are available here at jub Apollo we do very high intensive Milo ablative transplants using total body radiation for a pediatric patients adult patients we do autolus allogenic bone marrow transplants and sibling or unrelated donor Registries we collect donors from datri or International from German Registries we have done many transplants and we do a half match transplants to an extent we moved ahead further doing the tel depleted in order to reduce the complications we do a specific other modalities and uh to to prevent a relapses we use specific cell therapies called donor lymphocytes and if there was a failures you could use a stem cell second transplant or a boost up so all these complicated procedures are done and we have now completed 150 bone marrow transplant at a poo ju Hills we’re very proud to introduce extracorporal photopheresis is the new Avenue for preventing any graft versus host disas so we’re stepping every year to have a new things adding onto a basket and moving on to a very complex uh uh transplants as well

Closing Remarks
thank you thank you so much ma’am and I hope I’ve asked covered everything ma’am if at all I’ve missed out please uh explain us so no I I think you covered most of the things we could sit here and talk the whole day about what is available many people think Leukemia treatment is expensive unfortunately it is expensive and you have to be very open to your doctor discuss your financial situations there are ways you can deal with cut down the cost there may be a small risk people take but some treatments can be delivered as an outpatient with a very close followup perhaps some patients we do an alternate day follow-ups as an outpatient in order to reduce their financial burden and have the little safety thank thank you so much ma’am and thank you dear audience and I would like to make a note so dear audience at all our Apollo Hospital centers We are following strict measures to ensure that you’re entering a covid free zone all our doctors our Frontline Warriors our staff a security staff our nursing staff housekeeping staff everybody are wearing a mask using glos sanitizing their hands and the desks and everything and so that you’re entering a safe Zone and even uh we do take your measures as well like take do your temperature check we even give a mask to the patients if at all you’re not carrying yourself and sanitize your hands before you enter our hospital all our premises are safety so you can be rest assured that you’re entering a CO free uh safe Zone and please don’t delay your treatments or your follow-ups because you might land up in serious troubles other than Co thank you so much ma’am for joining us and clarifying most of the questions that audience have asked we have covered everything and if at all your audience you have missed out anything the causes symptoms or the treatment options diagnostic options once the session is done just rewind the session and you’ll find your answers but still if you have any doubts I’ve already given Dr padja M’s profile Link in the text box on one click you can book appointment and get yourself consulted with Dr pja man and if at all you have still any doubts we will definitely leave an email ID in the text box as well so you can even get in touch with us through an email thank you so much ma’am and thank you dear audience for tuning in

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Introduction
Hi. I am Ashley and I have gone the last 10 plus years, almost 12 with a brain tumor. It’s been a journey, that’s for sure. I have gone through three brain surgeries. I have done a lot of different things along the way. just I feel like one thing after another. But all with all of that going on I’ve always had a positive mind through it all.

The Beginning: A Seizure and a Discovery
So I had just graduated from Oregon State University and spent the summer here in Portland, Oregon where I’ve been my whole life and I kind of was ready to get out try something new. So I had just moved down to Scottsdale, Arizona and I had been there about a month, I would say kind of looking for teaching jobs because my goal was to do elementary school teaching. I had a grand mal seizure on my way out one night. Like, just even thinking back, it’s like crazy because it’s been so long now. But I had like I mean, other than like, things throughout my life nothing in relation at least medically, to this. So it was very like out of nowhere. Never had it before. Very confused. So what happened from there was I went straight to the hospital down there. And knowing that I see all my family and friends were still back up in Portland so it was kind of hard on them, which I remember thinking even in the hospital, like Oh my gosh, like my parents I feel so bad like they’re going to be worrying like, what’s going on? That was just the beginning But for the most part it was a lot of MRI, CT scans and trying to determine what exactly they found when they did it trying to figure out why I had the grand mal seizure at the time and they discovered it was a large mass in my left temporal lobe right here. And it could have been many things. So they had decided to do a biopsy, like a little mini surgery to learn more. And so I think a couple of days after getting there that’s when they did the surgery and found out that it actually was a brain tumor, a glioma, which is the type of brain tumor that starts there. It’s not like starting anywhere else. It’s only in my brain. And they needed to know more and do a like full on resection and remove as much as they could. That’s like the first step in any type of brain cancer. That’s like the go to kind of thing. So this is kind of like the beginning of it all at that first hospital. So I had the little biopsy surgery and kind of just was wondering like, okay, what’s next? Like, you know they knew at the time it was definitely a brain tumor but that was kind of it. We still didn’t know exactly what kind of there might be other things going on. We just needed to do better or bigger, I should say resection surgery from there.

Meeting the Surgical Team at Barrow
So we were sent over to St Joseph’s Hospital. It’s the Barrow Neurological Institute and it was in downtown Phoenix and better equipped for like massive brain surgeries. And I mean, people from all over the country would go there. So I met my main surgeon there, Dr. Nakaji and Peter Nakaji is his full name. But yes, he was absolutely amazing. He made me feel so comfortable. We had to go through quite a few steps beforehand because we I didn’t know that was going to be a awake brain surgery or I’d be asleep during it. And it’s hours and hours of surgery when they do any type of brain surgery because it’s very detailed and specific because you don’t want to mess up any other part of the brain. So we had to go through quite a few tests. I had to do a lot of tests which turned off that side of my brain and had me see what kind of like memory I’d be going through because it was located in my temporal lobe which is based on short term memory. But language speech kind of in that realm of things. So I went through all of that had quite a few meetings and luckily I did so well through all of that. I was able to be asleep through the full on surgery, which I was really like the surgery itself went absolutely amazing it ended up being a lot quicker. I mean, it wasn’t as long as they thought it was going to be because of the type it was It was just easier to resect and he was actually able to get about, I would say it was 95% of the tumor out there was still going to be tumor cells left. I mean, any type of brain tumor, unfortunately, is like incurable. There’s chances that it could be in remission for however long, but it’s just very like unlikely to get all of it out kind of thing. yeah, so that was kind of like what I went through for the like full on major surgery.

Early Recovery and Cognitive Challenges
And I did come out of it and had definitely a quite a few like deficits which I knew. I knew I’d be losing some vision in my upper right. I said I’m like like used to it. But the hardest part for me at least, was the memory especially after just going to college getting my degree ready to start my life my career and get things going. Of all things being wanting to be a elementary school teacher specifically, I really wanted to do first grade or second grade but I actually had to go to classes and be with that age group because of my speech and memory. I had to kind of like use different like games and puzzles and this and that to learn what everything was called because like, I knew what the words were but I couldn’t put it together with what things. Of course I would want to get it like a glass of water or I would be like Somebody give me a fork if I feel like I just make fairies. Like, I thought they were silly. I would always joke with stuff because I didn’t want to be a downer. Debbie Downer So I always like joke around with things, but it took a while. It took at least a year or two to kind of get back into motion of like not kind of standing out in front of people with my wording and memory. I mean, I still do have, short term memory loss where I it kind of I think it mostly affects me because before all this like in in college especially I would always get called out because of how good my memory was. Like I had a photographic memory and was like just read once I’m good to go kind of thing. So I kind of lucked out in that realm of things. And so some of my friends joke with me, they’re like Oh, now you have a normal memory but it’s not trust me, it’s not. It’s definitely like a struggle but it’s something I can deal with and like have work to, like live with and, you know, only make it better. that’s kind of how it was for since it happened and whatnot.

Diagnosis and Watch-and-Wait
But I had the surgery that 2012 or January 2012 and they determined it was a grade two oligodendroglioma which is one of the major types of a brain tumor. So at the time because it was a low grade I had a good surgery. We decided to do a watch and wait period instead of going directly to chemo radiation just to kind of see how it go on. So after the surgery I didn’t have to do anything once I was kind of like getting myself back to feeling better. We ended up for my parents came home, back up to Portland and I had to as well because as much as I wanted to stay there and teach and live my life, it just wasn’t going to happen. Unfortunately, just because of everything I was going through and I needed support around me. So I moved back up here and was just going through whatever I could to work on my memory system and just kind of recovery from that and till it did grow back in. It was at the very end of 2016, early 2015. I didn’t necessarily feel the regrowth happening, but I was having so many deficits in general just from the surgery and the tumor itself to begin with that. And luckily, you know, I do get MRI’s pretty often so they were able to see something going on at the time. At the time I did have migraines, but it wasn’t as bad as it ended up becoming.

Rebuilding Life and Facing Regrowth
So I would say like in the to two years or so before the regrowth happened it was a lot of just focusing on getting better and then kind of learning to just become this new person kind of thing. I mean, there was things I would never be able to change. That’s just how it was. But there was also with memory it was, you know, just kind of teaching myself and learning words again. And I was lucky. If I look back now I didn’t have like the nausea that I do now. And there’s very, like things there’s a lot of things at least that I am grateful for, that I like in life. It’s kind of weird in the sense like before this all happened I kind of looked at life in like a view of I’m going to do this and that, and I have all these life goals and whatnot, and I feel like I now look at life differently, where little things around me mean so much. And just the simple things in life are like amazing to me, you know?

Deciding on Treatment: Chemo and Radiation
So once they discovered that there’s at the time they weren’t exactly sure if it was regrowth or just something popping up that they were curious about. So they kind of wanted to do multiple like MRI’s, like more put together than normal for about, I would say two months because it is like it was March when we finally decided like, okay, it’s treatment time. And that’s when we had the talk with the doctor about doing chemo and radiation together this time which is kind of like the known treatment when this kind of stuff happens because we’d already done a massive resection and it was kind of that time and again, it’s like I already had it in my mind that this was very possible. So I didn’t have that like surprised look or anything like that. I was again kind of like, okay this is the this is the plan. This is our going to do it. I’m going to get myself ready and I’m going to beat it like I always have. Like, that’s like the weird thing. People kind of ask me about is like, aren’t you like, nervous? Aren’t you worried? And obviously I am but at the same time I’ve never had the view of like this is going to like and me, as weird as that is because I mean I’ve already outlived like the average life expectancy and it’s I don’t know this is like kind of a crazy thing, but I haven’t really met anybody younger than me. That is like lived this long as hard as it is. And I almost at least tell myself that positivity has such a massive effect because at least for me just having that mindset and not even like thinking about death at least has done more than I have asked for.

Chemo-Radiation: The First Round
So after kind of getting it all put together it was going to start with the Temodar which is the chemo that I luckily wouldn’t have to do at the hospital. It was like pills for that I had and I would take that every night during the first section of doing chemo and radiation together. So I’d be taking the chemo every day and then I’d be doing radiation Monday through Friday for six weeks and that honestly, like for the most part, it started off well. It wasn’t probably till the like halfway through when I started getting like crazy tired did a lot of like bed rest for sure. So I started like a little blog to kind of keep everybody up to date on how I was, what things were like. And so and that was really fun. So once I did the six weeks of chemo and radiation I had a 21 day break where I wasn’t on anything and it was right around my birthday. My birthday’s in May. That was really nice.

High-Dose Chemo and a Scare
But then once I had to go back on my six month like round of a like way higher dose of chemo where it was only I want to say five days. The first or the first five days of each month. So it wasn’t like every single day. It was a higher dosage of it but only five days for six months. But I had to stop it after the fourth month in September. At the time times that was right after I had finished doing it I had a very bad reaction and they weren’t exactly sure like why this happened. It’s not common or anything like that. But it was it was really bad. I had my whole body break out into like a hives. Look, I couldn’t move my body. I ended up in the hospital and they at the time just said, okay, we have to stop it. There’s no way we can continue this. And I all like I was scared thinking like Oh no, like, is that going to work still? Like, do I need to finish it? Like, so I had that when I like in the back of my head just being like, worried and not exactly sure what to expect. But luckily on the good side it slowly went away after like not having got in my system anymore. So I think what they determined is my body kind of just said, no, we’re done. Like we can’t take it anymore which is it’s a bummer. But like at the same time I had a good like overall result at the end. So once that kind of came through it was like it was all worth it at that point.

Side Effects: Hair, Headaches, and Heartbreak
So that was again it was a mix of chemo and radiation. And so I’m not sure it was really giving me like the nausea, the aches, the pains. And that’s also when I started getting like horrible headaches, migraines. They have a feeling it’s not necessarily related to like that type of head pain but more like nerves and nerve damage that was going on because it was only on this side where everything was like going down. And I had a alone with the the sickness and the nausea and just the all of the stuff. I lost my hair in is very unique way because it wasn’t the chemo that did anything to me because I thought, you know most of the time it’s chemo that kind of has the hair loss. But I was lucky in that sense that the chemo that I was taking did nothing but the radiation on my head did. And I want to almost say it was in the perfect spot as weird as that sounds because the top part stayed on and the bottom part stayed on but in a very precise loop around the middle of my hair was gone. It was like a huge part of my life that was not expected. So when I was going to go through chemo and radiation I actually at the time when I found out that there was regrowth I was pregnant. I had just found out I was pregnant. But unfortunately I did have a miscarriage shortly after. And again, it might have been meant to be or just from like the stress I was going through, but that was really hard. And I think looking back, that’s kind of why I didn’t take the option of like saving my eggs. And I kind of just told myself back then that if it’s meant to be, it’s meant to be, but I’m just not in the place right now to, like, go through that and wanted to kind of you know, get the tumor done before anything.

An Unexpected Miracle: Becoming a Mom
So I kind of never really even expected to be able to have kids kind of thing. I knew I could, but it was very unlikely believe it or not, like a year after going through the chemo radiation I got pregnant and that literally, like blew my mind and was again like the happiest I’ve ever been, the greatest gift of my life. he my son his name is Brody is definitely like what keeps me going every every day, no matter what he’s what I fight for. So but after that I would do my MRI’s about I want to see it back then probably every three months for about maybe the first year. And once that got kind of cleared, like everything’s good, no regrowth every thing is like kind of like down rather than up, like the cancer cells at least. So everything was looking good. So for about six or seven years like in remission, which again I’m very thankful cause I mean, that’s that’s a long time in the whole like realm of range. There was no changes in my memory or deficits that had changed at this point in time. So I was doing well for the most part and kind of just going with the flow and enjoying what I could just go on with it.

A New Scare in 2021–2022
So December, right? So I have my MRI’s twice a year. So December 2021 on my first call because that was kind of during the COVID era. But so I had my doctor call me on the phone to go over my results of the MRI. And originally he was like You’re good. it’s always kind of short and sweet, like, you’re good don’t say anything. And that’s what happened at first. Then the next morning he calls me again and said he wasn’t exactly sure if it was like dead cells or tissue that was kind of popping up or like what exactly it was. But he did want to kind of like feel it sooner than later. So it was a very hard time, kind of just watching waiting and kind of like all right, like, what is this? Is it just like a scare or is it regrows? Like, what is going on here? And then once they did that second MRI is when they kind of said Yeah, it’s definitely something. We’re not exactly sure what we need to do a surgery again. And this was not a massive surgery like before. This was another type of small biopsy to kind of determine what’s going on. Has it changed? Has anything else happened? So that’s what we ended up doing about a month, month and a half later in April. Yes, it was in April 2022. That’s when I had my third brain surgery. That one actually went pretty well. It was short because there wasn’t much going on and so I was only at the hospital I want to say maybe like five days or less even. And I again the surgery went really well. And this time was different, though because I now had a son and somebody that, you know I, you know, is is my world and my number one I mean, even with my cancer and like everything I’ve been going through he will always be my number one no matter what.

Updated Diagnosis and Rare Findings
But once I got the results from the surgery is when it was like the biggest relief yet. Kind of like not a good thing because obviously I don’t want to hear there’s regrowth. Obviously, like that’s not a good thing. But on the good side of things, there hasn’t been any type of a higher grade that’s gone into it which is very rare, especially after going through radiation, chemo and just over the years especially in brain tumors they normally will grow into a higher grade over time. I always like in the back of my mind, knew that was something to be prepared for, but to hear that it’s still a low grade. So much relief was like going off and kind of made me like more relaxed even though it’s like not a good thing to go through at all. The one thing that like threw me for a loop was the fact that it was no longer considered a oligodendroglioma brain tumor, which that’s like what I’ve always looked into and learned about. So when they said, Nope you don’t have an oligodendroglioma anymore, you now have a grade two astrocytoma with a CH one mutation which probably makes no sense right now but that’s what I thought too. I’m like, okay, what is this? They still thought it was an oligodendroglioma but they did say it’s kind of rare that you don’t have the one p 19 Q co deletions which is more so a part of that. So now since all these changes they’ve made because I don’t have that I now considered a astrocytoma and the two main mutations that I have that have basically like caused a brain tumor is the Tp53 which is a gene or like a mutation that does a lot of or it causes a lot of cancers not just brain tumors, many others as well aside from tagging the news like, yes, you have tumors back it is still at a good level to deal with where normally in the past at this point I would probably have to go through my second round of radiation. And the weird thing with my chemo in the past is they still aren’t sure if I should ever try that type of chemo again just because of how it affected me.

Trying a New Chemo Path
But now with all of these other changes they’ve found a new type of chemo that’s actually used with a certain type of leukemia. Since my is at that level and still very slow with the growth they decided, you know what, we should try this because this might be something that is positive and could help you. There’s been a couple other people with my main oncologist one of my main doctors that’s had really good results with a few of his other patients and I was like, Yep I want to try. I will try anything and everything and even outside of the medical realm of things, I try to eat healthy and exercise seriously with coaching, cheer and being a mom. So doing all of that, I love yoga. That’s like my go to and just making sure things like around me 24 over seven are helping as well.

Living with Tibsovo: Daily Realities
So it’s going to be almost a year of going through all this is when I started the tibsovo that I take at night every night about 250 milligrams pills at night. And it’s been overall I would say, other than that. So the nausea was hard at first. I had to have my body get used to it. And so I would say after probably like four months or so I finally got to stop taking nausea medicine. And I still get the nausea here and there, but I’ve kind of like just learned to to live with it. And other than that just the head pain and the tiredness. That’s the other thing that hasn’t gone away is that I do get really like fatigue and it’s kind of hard to kind of put myself through things that were just so easy before. I will say it’s definitely stressful because it’s kind of like another watch and wait period of time because it’s not anything, you know like right here, right now. So I do have my MRI’s every other month and then I have my blood work done every month and my EKG is like I just kind of have to keep up and get all of that taken care of to just make sure things are going well. And so far so good. Usually by now it should have stopped the growth from what I heard and it hasn’t quite done that yet. It’s definitely slowed the growth for me, but it hasn’t like completely stopped it. So I’m like, great my next MRI will have a good outlook on that but there’s always a chance that if it does I might have to like start something else but I’m not going to like worry about that just yet and keep going.

Choosing Positivity and Purpose
Living with this for so long, especially this type of cancer and having so many good times with bad times as well. But I feel like having that positive mindset has done so much. Helping others is a huge thing for me for sure even if stuff like this does happen instead of kind of like putting myself down I try to think of the positives and like I’m not saying it’s easy. I’m not saying I enjoy having to do all this. It definitely has given me like the strength and just the fight again

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so this videos on brain tumors and unfortunately there’s a lot of information that is fair game as it when it comes to brain tumors but fortunately for you if you organize it with some sexy dirty USMLE mnemonics it’s really not that hard this is gonna be free points for you on test day and it’s a huge section of Neurology anybody who’s flipped through first aid knows that neurology is a very very long section lots of information that you need to know but we’re gonna simplify it for your studying pleasure so in this video we’re gonna talk about brain tumors when we talk about brain tumors you need to separate them into the tumors of adulthood or the tumors of childhood and I’ve done that for you here tumors of adulthood include glioblastoma multiforme a oligodendrocyte OA tarry adenoma and schwannomas children tend to get different tumors and they include pilocytic astrocytoma medulloblastoma ependymoma and craniopharyngioma and pinny Aloma pineal OMA that’s a hard one to say we’re gonna start by talking about the tumors of adulthood so we’re gonna focus on the left side of this chart as I go through the video today we’re gonna talk about just in general what you need to know about the tumors what you’ll see on histology and then I’ll wrap up by giving you the mnemonics after we cover all the adult tumors we’ll transition into the tumors of childhood and we’re gonna just simplify everything I’m really excited to share with you this video because it’s very very high yield so this is a slide that you’ll see on most of these tumors again we’re gonna talk about what you need to know just generally speaking what you’ll see on histology and then I’ll give you my favorite mnemonic so we’re gonna get started with glioblastoma multiforme a so this is our first tumor of adulthood and what you need to know in general are that these are highly malignant tumors so they’re very aggressive very invasive highly highly malignant and they tend to cross the corpus callosum so they’ll cross the midline when you see them on radiology and this is pretty unique to this tumor so I’m gonna show you the picture on the next slide but if you see that it’s pretty classically glioblastoma multiforme a on histology you’ll see something referred to as quote pseudo pallas ating tumor cells and these stain positive for GF AP or G fab so here’s what a glioblastoma multiforme it looks like and as you can see if you know where the corpus callosum is which hopefully by this point in your career you do this tumor crosses the midline and it creates what’s called the butterfly appearance because it’s sort of symmetrical on both sides of the corpus callosum so glioblastoma multiforme a if you see anything resembling a butterfly or anything crossing the midline in the brain it’s gonna be a GBM so if we come back to GBM my pneumonic is glioblastoma multiforme a so he just changed the B to a P and what does that tell us well g4g fat positive P for pseudo Pallas ating cells and M for both midline and malignant so we’re gonna keep it stupid simple here GBM glioblastoma multiforme a I say glioblastoma multiforme AGP m4g fab pseudo Pallas ating and midline malignant that is your glioblastoma multiforme a so we’re already one tumor done you need to know everything that I said but if you use the pneumonic it beautifully summarizes all the high-yield buzzwords for you so if you see any mention of that stuff on exam day you know that it’s a glioblastoma multiforme a so don’t get bogged down dirty us emily is gonna keep this simple our next tumor is the oligodendrocyte on G so you see things that are known as chicken-wire capillary patterns you see fried egg cells and you see these tumors tend to be calcified grossly so this is really a big one for just histology there’s no general knowledge that I think is high-yield for us Emily or complex the reason that they’re called fried egg cells is because they have these classic round nuclei with clear cytoplasm and it’s sort of like if you fry an egg you see that the yolk is very clear you know clearly defined but it’s surrounded by the clear cytoplasm which would be your egg whites if you were to fry an egg so I don’t necessarily agree that this looks like a fried egg but that’s what pathologists and histology is call it so that’s what we go with the round nuclei clear cytoplasm those are termed fried egg cells so if you haven’t guessed yet our mnemonic is gonna be Oleg oh dendro glioma because all of these buzzwords have something to do with eggs so the chicken-wire capillary pattern well chickens lay eggs the fried egg appearance that’s a No and you get your calcium if you eat you know a nice hearty breakfast with eggs so calcified tumors Oh Lego dendro glioma instead of oligodendrocytes all you need to know for a Lego dendro glioma so if you’re cool it’s that you already know two tumors we’re crushing cruising our way through this list let’s keep the momentum going so we’re gonna talk about meningiomas next so meningioma are benign and they tend to be superficially located because they occur on the meninges and if you think about the anatomy of the brain the meninges / lie the superficial aspect of the brain so it’s no surprise that a tumor that originally arises from the meninges will be superficially located these are arachnoid in origin and think about the arachnoid mater in order to make the connection between their origin and the fact that it is a meningioma so it’s a tumor of the meninges on histology you’ll see similar bodies and spindle cells and I’m going to show you on this slide what this all looks like so you can see at the top portion of these slides on CT scan we see that the tumors are very superficially located because again they’re extensions of the meninges so meningioma meninges is in the name you can see at the bottom of this slide I’m showing you what a Sumomo body looks like so some omma bodies are unique to just a few tumors in the body and meningioma czar one of them now how do we remember all this right dirty’ us Emily what is your sexy sexy mnemonic for keeping this simple in my brain well you need to say men have problems with PSA so men for meningioma the first three letters of the tumor and men have problems with elevations in PSA because when they get BPH they have an increase in their prostate specific antigen so that’s what PSA stands for if you haven’t heard about that yet you certainly will as you move forward in your career but men have problems with their PSA so a PSA is our pneumonic so pee for Sumomo bodies s for spindle cells an a4 arachnoid origin if you can remember those three facts about a meningioma that’s everything that you really need to know or at least that’s everything that’s very high yield if they ask you a question about meningioma x’ that’s not one of these three things not p naught s not a then it’s not worth the brain space to memorize but that’s what we do here at dirty USMLE guys we keep this stupid we keep this simple three tumors down some more to go let’s keep it rolling hemangioblastoma probably one of the easier tumors to remember so this is of blood vessel origin it’s an eco producing tumor so it can cause secondary polycythemia it’s associated with von hippel-lindau syndrome very very high yield to know that and on histology you’ll see thin walled capillaries so no surprise the mnemonic we’re just breaking down the word for you oftentimes if you’re confused on us Emily comlex or even your in-class exams all you need to do is look at the word to figure out what it had you know like what the answer is so hemangioblastoma so heme for blood angio angio means blood vessel and blastoma is sort of describing the appearance grossly of the tumor so heme for blood so these are eco producing tumors they’re for blood eeep oh you know eople causes polycythemia so that’s a disorder of blood so heme angio means blood vessels so these are of blood vessel origins and literally when you look at the histology you see thin walled capillaries and then black stoma is irrelevant so we’re just breaking down the word to help remember this one sometimes it’s not worth memorizing a mnemonic heme angio blastoma blood blood vessel blastoma and then just to take it one step further to remember the association with von hippel-lindau syndrome sometimes instead of saying von hippel-lindau I say von eople endo because it’s sort of the same pronunciation that reminds me that not only are Heba angio blastoma associated with von hippel-lindau syndrome but they’re also associated with Ipoh and they cause secondary polycythemia so keep that stuff in mind very very high yield associations hemangioblastoma we’re gonna talk about pituitary adenoma sneck stand this is probably the highest yield tumor on this entire slide in this entire section so let’s get right into it with pituitary adenoma so you can have one of three forms of the tumor so it can be a lactate Rauf a Samana troph or a non-functional pituitary adenomas so what the hell do these words mean relax better break this down lacta troughs refer to one type of pituitary adenoma and specifically it’s a pituitary adenoma that perdu is prolactin hence the name prolactin oma so in a prolactin oma which is just a subtype of pituitary adenomas which is termed electa trophic pituitary adenomas aka a prolactin oma it produces prolactin and because of the inverse relationship between prolactin and FSH any increase in prolactin will decrease your FSH which will manifest as a certain very classic set of symptoms so what does elevated prolactin cause and likewise what does decreased FSH cause so in a female you’ll get things like Galacta Riya and amenorrhea all right in men however you’ll get gynecomastia and decreased libido because you’re inappropriately producing elevated levels of prolactin and you’re shutting down FSH so these are very classic symptoms that you should be on the lookout for if you see that constellation of symptoms in the clinical vignette chances are it’s a pituitary adenoma and the sensitivity for it being a pituitary adenoma becomes even higher if they have other symptoms like headaches etc so that is a pituitary adenoma but a very specific subtype of pituitary adenomas called a prolactin oma now let’s talk about the somatotropin pituitary adenoma so the somatic trophic pituitary adenomas could be a tumor that produces one of four substances it could produce growth hormone it could produce TSH it could produce ACTH or it could produce FSH or LH so no surprise here these are all hormones that are secreted by the anterior pituitary okay so when we talk about these hormones if the pituitary adenomas is a somatotropin dit produces growth hormone you’re gonna see clinical constellation of symptoms consistent with gigantism or acromegaly likewise if it’s a somatotropin do sis TSH you’ll see things like hyperthyroidism if it’s ACTH ACTH producing you’ll see Cushing’s syndrome and then FSH LH you’ll see the same set of symptoms that you should see if you just understand the physiology behind these hormones so my recommendation before you kind of memorize this and go through this lecture is to understand what these hormones do so go through the endocrine section first because it’s extremely high yield to be able to make that connection so if you have a clinical vignette and the patient has tachycardia you know diaphoresis but headache and there’s something seen on the CT scan that it sounds like hyperthyroidism but you see this tumor so you got to connect the dots and say this is a matter of trophic pituitary adenomas that’s producing TSH so that’s how you approach these problems so somatotropin hormones that come from the anterior pituitary and the symptoms are exactly what you would see if you just had elevations in any one of these hormones so not too difficult to understand the non-functional pituitary adenomas don’t produce hormones hence the name non functional so what kind of symptoms will you see on test day well you’ll see things consistent with Mass Effect and Mass Effect refers to headache and bitemporal hemianopia so the bitemporal hemianopia is the symptom that you get when you compress the optic chiasm and because of the location in the pituitary the pituitary adenomas has a tendency to compress the optic chiasm and caused by temporal hemianopia so right now I want you to pause this video and go on Google and Google bitemporal hemianopia and I want you to see what that changes in the visual fields because if they describe what you see on google images when you google bitemporal hemianopia they’re probably hinting at a pituitary adenoma so make sure you understand how the visual field changes if the buzz word is bitemporal hemianopia aka a non-functional pituitary adenoma compressing the optic chiasm and then obviously headache because you have mass effect you have a tumor growing in the brain kind of subtly pushing the brain in a certain direction so that is Mass Effect for a non-functional pituitary adenomas so how the hell do we remember all this stuff that’s the question this is really easy eyes remember add Anoma so add Anoma because you’re adding on all of these hormones in the brain or you’re adding on the actual mass of the tumor to create mass effect so pituitary adenomas x’ add hormones into the picture like prolactin GH TSH ACTH FSH LH or they add their mass into the picture to create headache and bitemporal hemianopia very very high-yield tumor to understand I think I simplified it well for you but make sure that you understand everything on this that is pituitary adenomas we’re gonna wrap up the adult tumors by talking about the famous schwannoma so the schwannoma gets a lot of love on tests because it has a very classic presentation so it occurs at the cerebellopontine angle so Google that really quickly so you see where that is but when you have a tumor sitting in the cerebellopontine angle it has a tendency to affect cranial nerve seven and Creole nerve eight so your facial nerve and your vestibular cochlear nerve so the thing that you need to know about schwannoma is in addition to which cranial nerves they affect is that if they’re bilateral you want to think neurofibromatosis type two so if they’re unilateral it’s just in a coma existing in isolation but if you have to chew on ouma’s right bilateral schwannomas you should think of nf2 that’s very very classic Association very very high yield to know that on histology you need to memorize that schwannomas rs.100 positive so if you need a mnemonic you need some dirty USMLE lovin just remember schwa Anoma so the SCH w very very high yield s for s 100 c4 cerebellopontine angle and the h and the w tell you which cranial nerves are affected so the H hearing is affected that’s cranial nerve eight and the W winking is affected that’s cranial nerves seven so very very high yield schwannoma SCH w just remember what their stand for s 100 cerebellar Ponty and hearing and winking that’s cranial nerve seven and cranial nerve eight if you have bilateral schwannomas it’s an oral fibromatosis type two very high yield association so that’s all of the adult brain tumors those are the hard ones guys so that’s done we’ve covered all the hard stuff you have mnemonics for all the hard stuff the childhood tumors are a lot easier and the reason is is that childhood tumors you just need to know maybe one or two buzzwords associated with each tumor and if you know those buzzwords you are golden you are absolutely golden they don’t ask a lot of this on exams so we’re just gonna cover the buzzwords so we’re gonna do this all in one fell swoop so I’m gonna put through the buzzwords on the right side of the slide and then I’ll go through them one at a time and explain how you remember this so the tumors are pilocytic astrocytoma medulloblastoma ependymoma craniopharyngioma and Pinney Aloma okay what you need to remember corresponding to the tumor is exactly a cross right is that in pilocytic astrocytomas you get things called Rosenthal fibers and they stain positive for G fat okay so how do we remember the association between pilocytic astrocytoma and Rosenthal fibers right so random the way that I think about this and you sort of need to be a sports fan to understand my pneumonic here is that there is a sports agent named Drew Rosenhaus so I remember Rosen for Drew Rosenhaus and then in astrocytoma I think of the Houston Astros and even though he’s a football agent he represents football players I think of him as representing players who play for the Houston Astros so that is Drew Rosenhaus from rosenthal fibers representing players on the Houston Astros in astrocytoma so very very high yield to know that Association that’s my silly sports mnemonic sorry if you’re not a sports fan next for medulloblastomas you need to know about Homer right rosettes so what the hell how do we remember this again sorry but you kind of got to be a sports fan for this one if you want to hit a homer run or a home run out of the ballpark you need to blast the ball so you blast the homer run or the homer right rosettes so for Homer right rosettes you blast the homer run out of the ballpark that is the high yield mnemonic for medulloblastoma for ependymoma you get something called perivascular pseudo rosettes so one buzzword to know here perivascular pseudo rosettes so I sort of create a story in my mind and I think about my momma right my mom ependymoma append a momma append a mommy however you want to do it and you forget that it’s your mom’s birthday so you give her a rose which is pseudo rosette but since it’s pseudo rosette its pseudo means sort of or kind of or like somewhat so it’s pseudo rosette you you gave your mom a rose to somewhat make up for the fact that you forgot her birthday that’s just how I always remembered that it’s sort of a stupid story but it absolutely works so if you get a pen demo aka append Amami Penda mama just remember that you sort of forgot her birthday so you gave her a sort of makeup gift which was a sort of rose AKA pseudo rosette so that’s ependymoma for craniopharyngioma all you need to memorize is that these are remnants of wrath use pouch that give rise to craniopharyngioma x’ so there’s no pneumonic there it’s just a brute memorization if you see wrath key anywhere on your exam the answer is current craniopharyngioma like don’t don’t think twice just pick it that’s the answer and fourpenny Aloma it causes paranoid syndrome but you remember the peas Pinni Aloma for paranoid syndrome look into what that entails exactly i would google it it’s a little lengthy for an explanation in this video but the association itself between pineal Ouma’s and paranoid syndrome is extremely extremely high yield so know that association but guys and gals that’s it you now know all of the brain tumors that occur in adulthood in childhood there’s no reason to go through any other resource and learn anything else about these freaking tumors they’re really annoying to learn and if you’re not gonna be a neurologist you really don’t have to know that much about them just know the buzzwords that I’ve presented to you in this video remember to check out the description of this video give us a follow on Twitter if you want us to make a video about a certain topic all you got to do is tweet at us and I’ll feature your tweet in the next video when I create the video for the topic you requested

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the human imuno deficiency virus or HIV is a retrovirus that infects CD4 T lymphocytes among many other cells leading to the destruction of these CD4 T cells and thereby impairing cell mediated immunity and increases the risk of cancer and opportunistic infections HIV 1 is the most common species worldwide HIV 2 is restricted almost completely to West Africa

Viral Structure
the structure of the virus is that it’s uh icosahedral meaning a polyhedron with 20 Faces with a conical capsid a protein shell of a virus the capsid contains two strands of RNA the capsid also contains two enzymes essential for HIV replication the integr and the reverse transcripts the cset also contains two strands of RNA which holds the hiv’s genetic material hiv’s RNA is made up of nine genes which contain all the instructions to make new viruses three of these genes gag pole and EnV provide the instructions to make proteins that will form the new virus particles consisting of the core proteins the enzymes and the envelope glycoprotein the outer shell of the virus is called the envelope and is made up of lipid layers which are covered in spikes of the glycoproteins I mentioned here you can see glycoproteins gp41 and gp20 these glycoproteins allow the HIV to lock onto the CD4 receptors on the cd4t cells and enter the cell so let us take a look at how the virus does do this and also learn about the life cycle of the HIV um virus by looking at some key steps

Entry and Early Infection
the HIV virus gains entry into the cell you know following sexual intercourse which is a major cause once the virus is within the body they will infect immune cells which have CD4 receptors on the surface the main cells here that contain the CD4 receptors are the cd4t lymphocytes when HIV makes contact with a CD4 cell the GP 120 Spike on the surface of the HIV lock onto the CD4 receptor and another co-receptor ccr5 or cxcr4 this first step is called attachment and this step essentially will result in the fusion of the viral membrane with the cell membrane

Fusion
the second step of the life cycle is Fusion the process of fusion allows the HIV capsid to enter the CD4 cell the gp41 protein is used to fuse the HIV envelope with the cell wall the capsid releases the viral RNA the reverse transcripts and the integr as well

Reverse Transcription
the third step is reverse transcription here the HIV uses its reverse transcriptase enzyme to convert the RNA it contains into a proviral DNA inside the cell so now you have the double stranded blue DNA which is the viral DNA

Integration and Latency
once this is done the next step is integration the hiv’s integr enzyme attaches itself to the end of the proviral DNA strands and Carries the viral DNA into the cell nucleus once the proviral DNA enters the cell nucleus it binds to the host DNA and then the HIV DNA strand is inserted into the host cell DNA after the proviral DNA is integrated into the DNA of the host HIV either continues to use the body’s own cell Machinery to replicate or it will remain dormant within the cellular d DNA this stage is called latency and the cell is described as latently infected

Transcription and Translation
the next step is transcription when the cell becomes active the HIV uses the host enzyme RNA polymerase to read the HIV Gene to make messenger RNA and genomic viral RNA this is called transcription focusing on the mRNA the next step is translation the messenger RNA provides the instructions for making new viral proteins including structural proteins and the viral enzymes the viral genomic RNA and these viral proteins will prepare to be assembled

Assembly, Release, and Maturation
in assembly and release what happens is the enzymes and the HIV RNA will begin to assemble into the new viruses at the cell wall after the new virus is assembled it must leave the cell by pushing through the cell wall the virus must take lipids the fat from the cell wall to make the surface glyco proteins including the gp120 and the gp41 shortly after the virus is released from the cell the viral proteas actually cleave some of the precursor proteins which will help form the mature capsid as we know it this makes the virus mature and infectious the cycle can continue this HIV virus can then uh infect other people or infect other cells

Routes of Transmission
the root of transmission of the HIV virus is via sexual intercourse majority of cases it can also be transmitted parentally so through the blood or vertical transmission from mother to baby

Immune Response and Pathophysiology
so we looked at the life cycle of HIV and how it infects a CD4 T cell and how it also replicates within these cells but what does the body actually do when HIV infects the cd4t cell how does the body’s immune system you know respond to the HIV infection next we will focus on the pathophysiology and the na natural history and progression of HIV so what happens is you have these dendritic cells which are the first to recognize a HIV virus and present them to the immune system to mount an immune response what they do is that they engulf the virus process them and then present them on their cell surface via MHC Class 2 they then travel to the lymph nodes and what’s called the GT gastric Associated lymphoid tissue carrying this viral particle where they activate or stimulate cd4t lymphocytes the CD4 T Cell will then activate B cells and plasma cells to produce antibodies against HIV CD4 T cells will also activate cd8 t- cells also known as the cytotoxic te- cells during this time the HIV continues to infect cells the only cells that can be infected by the HIV virus are those that have the CD4 receptor these cells as mentioned are the monocytes macras dendritic cells micral cells but more specifically the the T lymphocytes the greatest concentration of these cells is in the gut Associated lymphoid tissue and lymph nodes as the virus replicates within the cd4t lymphocytes it kills the cells and spreads again

Acute Infection and Seroconversion
about three to four weeks after the initial infection the HIV viral load increases and is detected the HIV p24 antigen is also detectable the HIV antibody is detectable in weeks 2 to 4 roughly and once this occurs this is called serero conversion when you get sereral conversion where you get presence of the antibodies as well as you get this increase in the viral load this causes what’s called COC conversion sickness or COC conversion illness which manifests as symptoms of acute HIV infection interestingly these symptoms are very non-specific and they include fevers fatigue myalgia rash headache fitis and lymp lymphadenopathy really symptoms of a standard viral infection which vary and are self-limiting and go away by up to 2 weeks so in summary the acute infection which are in the first uh weeks causes an increase in viral load of the HIV virus you get the presence of HIV p24 antigen you get presence of the antibodies against HIV which actually begin to appear between weeks 2 and four and you also get the cd8 T Cell being AC activated in this period you also get C conversion illness which can be very mild and even go unnoticed

Immune Control and Viral Evasion
only a small proportion of the infected CD4 T lymphocytes allow the virus to replicate and you know get released again these infected T lymphocytes usually Express MHC class one molecules with the viral antigen which essentially tags them so that they are recognized as an infected cell which allows the cytotoxic cd8 T lymphocyst them controlling the infection unfortunately as the HIV infects more and more cd4t lymphocytes they are able to form mutations in their genetic material which allow them to evade the immune system hide from the immune system and and they do this by downregulating the MHC class one expression essentially making it unrecognizable by the immune system HIV hides within CD4 uh cells where they remain dormant

Asymptomatic Phase
HIV infection will not really cause further illness for some years and this period is known as the asymptomatic phase which is roughly about 10 years HIV in infected CD4 remains dormant and slowly reduces the CD4 uh t- cell count the viral load of the HIV remains steady because the cd8 t- cell the cot toxic t- cell keeps their numbers in circulation uh at Bay in the asymptomatic phase the viral load and HIV antibodies are detectable and remember the CD4 count will slow slowly go down here during the asymptomatic phase CD4 T cell count and viral load tests can monitor the progression of the HIV disease

Disease Progression Over Time
looking at the two stages we have learned so far using this graph with time on the x-axis we can see the viral load will increase in the first few weeks during the acute infection but then drop and remain relatively stable because the immune cells such as the cd8 cytotoxic tea cell keeps it in check for around 10 years this is the asymtomatic phase until eventually after about 10 years if left untreated the viral load will begin to increase looking at the CD4 cell count from day one of infection the CD4 cell count slowly dwindles because as we have learned the HIV infect CD4 cells such as the CD4 T cells and slowly causes them to die during the asymptomatic phase here you have serero conversion illness where the body begins producing antibodies the B cells plasma cells begin producing antibodies by weeks 2 to four of the initial infection the cd8 T cells are created to destroy the HIV infected cells HIV levels begin to fall in the blood because of this and after a few weeks to months the viral load and CD4 levels will stabilize at a level known as the set point

AIDS Definition and Risks
HIV gradually reduces the number of CD4 t- cells in the body until the CD4 cell count Falls below 200 cells uh per millimet cubed when the t- cell count is this low they are at risk of developing uh AIDS also known as acquired imuno deficiency syndrome AIDS is defined by a CD4 cell count of less than 200 cells per millim cubed or if they develop an AIDS related illness when someone has AIDS their risk of infection increases their risk of malignancy increases as well as other comorbidities AIDS defining infections are very important once the CD4 cell count drops below 200 you are likely to develop certain infections some infections develop at a much lower CD4 cell count people with a CD4 cell count below 500 also develop AIDS uh defining illnesses including carpos saroma invasive cervical cancer and tuberculosis I have a separate video that goes into lot of detail into the AIDS defining illnesses please have a look

Screening and Diagnosis
let’s talk about screening and diagnosis of HIV so what you do is if you suspect someone has HIV you can do what’s called a combination essay which is basically looking at the HIV antibody as well as the presence of the p24 antigen if positive you can do What’s called the antibody differentiation essay which essentially will tell you uh which type of HIV um the person has either HIV 1 or HIV 2 if the combination essay is negative meaning there’s no HIV antibodies present you can check the HIV viral load by looking at the HIV RNA nucleic acid amplification test or naat if the viral load is positive you can also diagnose HIV because they have viruses in the blood if the viral load is negative then this person does not have HIV at that particular time

Baseline and Additional Investigations
other investigations for HIV once confirmed firstly you know you always want to get the viral load uh but you looking at the HIV RNA and this is to look at a baseline also performing t- cell subsets to establish a CD4 cell count you can also perform vile resistant testing at Baseline for blood count eu’s lft glucose fasting lipids check for latent TB performing a tuberculin skin test and interfer on gamma release assay hepatitis viral corology corology for syphus and other sexual transmitted infections corology for toxoplasmosis as well as cervical papia

Management Overview
the man management of HIV just briefly education is very important again the infection is treatable and a person can have a normal life educate them on safe sex condoms as well as educating them on the complications of the disease and the medications treatment involves anti- retroviral therapy and it’s important to treat the person right away and it is lifelong treatment monitor for complications specifically opportunistic infections that may arise AIDS defining illnesses as well as medication side effects I will have a separate video that will focus on the pharmacology of HIV and I’ll put the link at the end of the video

Summary
so in summary HIV is a virus that essentially infects CD4 cells such as your cd4t cells and what they do here is that they replicate within the cell or they can remain dormant what they will do over time is that they will deplete the CD4 count and when the CD4 count is depleted it will increase the risk of opportunistic infections treating person with HIV early with anti- retrov therapy is important thank you for watching

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Introduction
in the early days of the 1980s an unknown stalker was doing the rounds in the u.s preying mainly on young homosexual men one after the other they fell victim to illnesses considered to be quite rare until that time patterns began to emerge leading to the discovery of a new infection leading to the syndrome that would be dubbed the plague of the 21st century a plague that would carry with it the stigma of behaviors considered by some to be morally reprehensible hiv in today’s episode we will trace the origins of the disease from the first publicized cases in the u.s to the later research pointing to the first outbreaks across the atlantic along the way we will discover the truth behind the man still known as patient zero hiv and aids were not easily identified at the start it took time for medical researchers to piece together the clues that would lead to the identification of a new illness the first recorded event in that trail of clues was a morbidity and mortality report published by the centers for disease control and prevention on june 5th 1981. this report described five cases of a rare type of pneumonia pneumocyst is carinae or pcp this is a type of infection of the lungs caused by the fungus pneumocystis duravetsy which leads to difficulty in breathing a high fever and dry cough the patients were young previously healthy gay men in los angeles all of them showed signs of severe immune deficiencies within days doctors across the u.s submitted reports of similar cases to the cdc less than a month later on the third of july the new york times published an article about the outbreak of a rare cancer 41 gay men in new york and california had been affected by kaposi’s sarcoma an abnormal growth of small blood vessels that manifest itself with firm pink or purple spots on the skin it can become life-threatening when it affects the internal organs more and more homosexual men fell ill with rare conditions very often they were associated with immune deficiencies in january of 1982 some of the patients and their friends and families founded gay men’s health crisis this organization would become the first non-profit community-based hiv service provider but at the time they didn’t know what they were fighting against very soon it became clear that whatever was infecting u.s citizens was not only targeting homosexuals on july the 16th 1982 a cdc report featured three cases of pcp in heterosexual hemophiliac men hemophilia is a genetic condition which prevents blood from clotting in the 1980s patients suffering from it required frequent blood and plasma transfusions around the same time the first cases of a new disease were being recorded in sub-saharan africa in uganda this disease was nicknamed slim jim as it caused massive weight loss among its victims later that year the term aids was first used to identify the new disease it was the 24th of september when the cdc released the first definition of aids a disease at least moderately predictive of a defect in cell-mediated immunity occurring in a person with no known cause for diminished resistance to that disease gay men were in a group among which the disease was most prevalent but it quickly became apparent that they were by no means the only victims in january of 1983 the cdc recorded the first two female patients they were partners of men living with aids which suggested a sexual transmission of the disease firstly in may of 1983 two teams of researchers found the cause behind this new illness the first was a team headed by dr francois barcinussi and dr luke montagna at the pasteur institute in france they isolated a virus which they believed was responsible for causing aids which they called lav or lymphodenopathy-associated virus later that year dr robert gallo of the national cancer institute in the u.s cultivated lab specimens in his lab identifying it as a retrovirus this is a type of virus which can insert a dna copy of its genome into a host cell in order to replicate in june of 1984 dr gallo and dr montagna held a joint press conference announcing their discovery that a retrovirus was responsible for causing aids the french doctor called it lav gallo called it htlv-3 they later changed the name to human immunodeficiency virus hiv the acronym aids stands for acquired immunodeficiency syndrome and is the advanced stage of the infection caused by hiv hiv is a rather aggressive virus which targets the cells of the immune system making a person more vulnerable to other infections and diseases which are called opportunistic infections a healthy individual can contract hiv by contact with certain bodily fluids from an infected patient with detectable viral load most commonly this happens during unprotected sex or through the sharing of injection drug equipment a person who is hiv positive is considered to have progressed to aids when the number of their white blood cells of the cd4 type falls below 200 cells per cubic millimeter or regardless of their cd4 count when they have developed one or more opportunistic infections opportunistic diseases most commonly associated with aids which can often lead to the death of a patient include bacterial infections like salmonella tuberculosis and pneumonia less well-known consequences are fungal infestations like thrush and pcp however the weakening of immune deficiencies brought about by hiv can also lead to the onset of certain types of cancer for instance lymphoma and kaposi’s sarcoma as of today there is no cure for hiv however certain treatment regimens known as heart or highly active antiretroviral therapy can help patients live with hiv without it degenerating into aids and we’ll get into those a little bit later without this therapy people with aids typically survive about three years sadly if they contract a dangerous opportunistic illness their life expectancy falls to about one year patients who are hiv positive can live for 10 to 15 years without any noticeable symptoms and even if they manifest they can be easily mistaken for those of a less serious illness like flu when hiv degenerates into aids common symptoms include rapid weight loss diarrhea fatigue memory loss and depression again these symptoms are not exclusive to aids and can be related to other illnesses that is why the only certain way to diagnose hiv and aids is to get the appropriate test to avoid an uncontrolled spread of the infection the most common ways through which aids is transmitted are unprotected sex and the sharing of needles by drug users but there are other less common avenues for example a mother can pass hiv to a child during pregnancy birth or breastfeeding there have been cases of health workers being infected when handling hiv contaminated needles or other sharp objects particularly if they are not utilizing the recommended personal protective equipment a patient may also receive a transfusion of blood or plasma from a donor who is hiv positive nowadays this risk is extremely low because of the scrutiny that blood donations receive but there had been many cases recorded in the early 1980s before rigorous testing was put in place finally there is an extremely low risk of contracting hiv via oral contact for example if an individual is bitten by an infected patient or if two partners both with bleeding gums or mouth ulcers share a deep kiss hiv absolutely can’t be spread by insect bites physical contact air water saliva tears or sweat hiv can affect anyone regardless of sexual orientation race ethnicity gender or age however certain groups are at a higher risk of contracting hiv the records of the centers for disease control and prevention show that in the u.s certain demographics are more likely to get this virus according to 2018 cdc statistics gay bisexual and other men who have sex with men accounted for 69 of all new hiv diagnoses the next largest category was heterosexuals accounting for 24 percent of new cases followed by injection drug users at 7 records show that the incidence of new cases disproportionately affects ethnic minorities for example african americans are about 13 percent of the overall population in the u.s and yet they account for 42 percent of the newly infected hispanics are 18 of the population but account for 27 percent of the hiv positive people who identify as white are 70 of us citizens but they are just a quarter of the overall instant patience all things considered gay african-american men are the category at highest risk for contracting hiv representing 25 percent of all cases so let’s go back to the 1980s it was becoming clear to medical professionals and even part of the general public that this new disease favored certain groups defined as the four h’s homosexuals heroin addicts hemophiliacs and haitian immigrants the first advocacy group started to take shape in 1983. on may the 2nd people with aids staged their first public demonstration in san francisco in the following months patient groups issued the denver principles a charter stating their right to be involved in policy decisions and to be called people with aids not aids victims on the 22nd of november the world health organization held its first meeting to assess the global impact of aids by this date at least one case of the disease had been reported in each region of the world it took another couple of years though before aids fully entered the public consciousness first it was thanks to an indiana teenager on june 30th ryan white a boy living with hemophilia was denied admission to a local school he had been infected with hiv from a blood transfusion ryan went on to speak publicly against the stigma and discrimination that many aids patients experienced the other event was the death of rock hudson on the 2nd of october the legendary hollywood actor died of aids leaving 250 000 to help set up the american foundation for aids research or amphar fellow actress elizabeth taylor acted as national chairperson for amfar which gave a further boost to the disease awareness efforts the first few years of the epidemic and their impact especially on the gay community were recorded in the 1987 book and the band played on by randy schultz a journalist at the san francisco chronicle the book introduced a real-life character a gay canadian flight attendant who had succumbed to aids on march 30th 1984. thanks to his good looks charisma and field of work the flight attendant traveled across the country having a string of sexual encounters along the way apparently in a typical year he could have up to 250 one-night stands while researching his book schultz came across the cluster study published in the american journal of medicine with this study cdc investigators sought to drop a map of sexual encounters among several people with aids the study featured a diagram illustrating this network of relationships at the center of the largest cluster responsible for directly infecting eight patients this paper had identified one person as patient zero according to schultz this patient was ultimately responsible for introducing hiv and aids to the united states for years after schultz’s work had been published a medical dictionary still refers to patient zero as an individual identified as the person who introduced hiv in the united states according to cdc records patient zero an airline steward infected nearly 50 other persons before he died of acquired immunodeficiency syndrome in 1984. that airline steward was the canadian flight attendant we discussed earlier and his name was gayten duggar was born in quebec city canada on february 20th 1953. he worked for a period as a hairdresser in toronto before moving to vancouver there he realized his dream of becoming a flight attendant working for air canada while on duty he frequently traveled across europe the caribbean and the us with his favorite destination being san francisco gaiten loved to attend the annual pride parade but he flew to san francisco as often as he could enjoying many of his sexual encounters there gayton was 26 when he first displayed symptoms of ill health in this case swollen lymph nodes a year later in 1980 brown spots appeared under his skin gayton had them checked with a biopsy which revealed that he had kaposi’s sarcoma gaiton had to undergo several cycles of chemotherapy with all the side effects that go along with that from inconvenience to agonizing pain despite losing much weight and all of his hair gaiten continued to sport a cutting-edge look wearing fashionable headbands and designer clothing by this point the clinical community had linked caposis to the new disease targeting homosexuals it was referred to as gay cancer in a letter to ray redford a former lover and friend dugard described his mental state as he tried to learn more about the disease and to keep its symptoms at bay he wrote my mind is finding peace again you’re right i must upgrade my attitude towards a full recovery but you know there is always this storm that strikes you when less expected the cdc started interviewing gay men with kaposi sarcoma and soon realized that at least four of them had slept with gayten duger took part in this cluster study too cooperating eagerly and volunteering plenty of detailed information on the names and addresses of his previous partners the cdc made it clear to gate and that the new deadly illness may have been spread sexually according to schultz in november of 1982 gaydon duker was even confronted by a san francisco public health official about his sexual habits duga was asked to avoid having sex prevent further spreading of the disease but he flatly refused it was his right he said to do what he wanted with his body by that time duga had moved to san francisco permanently and he frequented the local bath houses looking for new partners his success streak was such to rouse the jealousy of other gay men in the area some even conspired to have him evicted from the town it was because of behaviors such as this that schiltz harshly branded duga as the quebecois version of typhoid mary eventually duga left san francisco and resettled in vancouver his body was now consumed with opportunistic infections the most serious one being pcp the fungal pneumonia the infection progressed inexorably gayton moved back to his native quebec city where he passed away on march 30 1984 aged just 31. the cluster study was published some weeks after his death all that remained of gayton’s lust for life was a circle at the center of a diagram it was connected to eight other circles la 3 6 8 and 9 and ny 3 4 9 and 15. gaten’s circle was marked by a zero the only thing is it was not a zero it was the letter o the cluster study marked its participant by location gate and dugar had been recorded as out of california or simply o for short randy schiltz’s work had many critics with cambridge historian richard mckay among them mckay points out that schultz had misunderstood the letter o for a number zero the diagram of the cluster study was not supposed to illustrate what may have been the epicenter of the pandemic in the u.s it was intended to find a link between two outbreaks of kaposi sarcoma and other opportunistic illnesses one on the west coast and the other on the east gaten o and a certain sf1 were the links between east and west the gaten just happened to be placed at the center some of the other interviewees in the study were as promiscuous if not more so than duga but they could not or would not provide as many details as the canadian steward hence his circle marked with the o appeared as more interconnected to other men that’s why it was easier to represent him graphically at the center of the diagram schultz’s editor michael denneny admitted that the two had overplayed the responsibilities of duga in the epidemic in order to make and the band played on more appealing they painted gayten as the villain of the piece patient zero the typhoid gary if you like who had introduced hiv and aids to the u.s the intention was ultimately noble increased circulation of the book to raise awareness about hiv as well as the stigma and indifference suffered by gay people with aids at the hands of authorities in the public but in doing so the book created the false myth of patient zero scapegoating gate and duga even if the canadian man was not an actual patient zero schiltz’s book makes it clear that he stubbornly continued to spread hiv through unprotected sex but that claim is disputed as well the cdc first stated that aids was sexually transmitted in january of 1983. gayten’s discussions with the cdc and the san francisco health official took place in 1982. duga’s behavior was certainly promiscuous he definitely lacked caution but it wasn’t as brazenly irresponsible as portrayed in the book he was not consciously infecting as many men as he could what really matters to us is that hiv in the u.s did not start with gayten it most likely cannot be traced to one single individual and most likely did not start in the late 1970s or early 1980s considering that hiv can take as long as 15 years to display symptoms many people could have been infected long before then in october of 1987 an article in the chicago tribune reported a story about tests run on samples belonging to a teenage male from saint louis the samples tested positive for hiv and in fact the individual had died from an aids-like condition in 1969. a nature article in 1990 found that tissue samples from a british sailor had also tested positive for hiv he’d died in manchester from pcp in 1959. more clues pointed to an earlier origin of the disease and to a location many miles away from north america in 1983 a joint belgian and american research trip to zaire now the democratic republic of congo established that a similar disease to aids was widespread there affecting mainly heterosexual men and women in 1987 medical journal the lancet found evidence of hiv-like infections in central africa dating back to 1959 researchers were closing in on the place of origin of this plague of the 21st century and it was sub-saharan africa one of the most credited theories on the origins of aids is the one dubbed cut hunter theory one of the proponents is microbiologist jacques paypal in his 2011 work the origin of aids he proposes a likely travel route from central africa to north america and the rest of the world hiv likely originated as a pathogen in primate populations most probably chimpanzees late stage infected chimps developed a syndrome called sid simeon immunodeficiency sometime in the early 1920s the virus jumped species this is when the virus somehow relocated from an infected ape into the bloodstream of a human the most likely candidate would be a hunter whose open wounds were infected by the chimpanzee’s blood the cut hunter in other words in the 1920s and 1930s french equatorial africa and the belgian congo enjoyed close trade and employment ties meaning that any infected individual could have traveled across highly populated centers via short boat rides spreading the disease further and further papa in fact found evidence of a disease similar to aids causing an outbreak in a railway camp in french equatorial africa in the 1920s and early 1930s hiv may have spread via sexual contact but also via irogenic transmission these are infections caused by doctors reissuing unsterilized needles travelers and sailors visiting central africa may have contracted hiv as early as the 1950s however paypal was able to establish with more certainty a link between zaire and the caribbean during the 1960s several thousand haitians were recruited to work in xayah it is possible that many of them became hiv-positive and carried the infection back to their country from haiti hiv made its way to north america by two avenues the transnational blood industry and sex tourism a study published in nature in october 2016 ascertained that blood and plasma collected from haiti by new york hospital was indeed hiv positive by cambridge historian richard mckay argues that haiti was a popular destination for american gay men looking for sexual liaisons from these two entry points the virus gradually spread to hemophiliacs heroin users and homosexuals and of course there are scores of potential haitian immigrants jumping the gulf to the united states the four h’s that we already mentioned through the effects of paypal mckay and other researchers it is clear now that the whole concept of duga as patient zero is more or less debunked the first outbreak of what could be called aids dates back at least half a century before and it went completely undetected before it swelled into what appeared to be an unstoppable pandemic since the beginning of the epidemic 76 million people have been infected with the hiv virus and about 33 million people have died of aids-related infections luckily advances in medical science have made it possible for hiv-positive patients to live much longer than ever before what used to be a fatal disease has now become a chronic illness it can’t be cured but it can be managed through the regular use of antiretroviral drugs the first treatment indicated for hiv was approved by the fda in 1987. in july of 1996 the 11th international aids conference established heart as a breakthrough approach leading to a drop in morbidity and mortality advances in other disease areas have also made it possible to prevent or treat the symptoms of the most common opportunistic illnesses however hiv and aids are far from being completely defeated at the end of 2019 about 38 million people were estimated to be living with hiv across the globe during that same year 690 000 people died of aids three hundred thousand of them died in eastern and southern africa alone despite some advancements in treatment rates sub-saharan africa is still the region suffering the most from hiv and amongst the infected about three-fifths are women and young girls according to unaids the joint united nations program on hiv aids the progress of the hiv crisis is related to the low supply of antiretroviral therapies naturally this is a situation which may be exacerbated by the concurrent pandemic we are now going through with covert 19. but unaids identifies another set of reasons gender inequalities lack of access to secondary education for girls scarcity of sexual and reproductive health services there’s also the ongoing stigma which prevents hiv-positive people and at-risk populations from seeking treatment and preventative advice now we’ve mainly focused on the american hiv story but here at today’s conclusion i’d like to bring things closer to home in 1987 millions of households in the uk received an information booklet on the risks of hiv and aids the booklet was tied to an effective tv ad campaign and it used frank language on the matter of transmission via sexual intercourse the tagline of this department of health campaign was don’t die of ignorance it drove the point home during any public crisis knowledge and the responsible behavior that grows out of it are really key as you’ve seen today ignorance about the disease caused millions to die but ignorance and its brother prejudice can also isolate condem and taint the memory of those who don’t deserve it so i really hope you found today’s video interesting if you did please do hit that thumbs up button below don’t forget to subscribe as always thank you for watching you

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What if I told you that COVID 19 could trigger
an autoimmune disease in someone who never had symptoms before? Or even worse, what if your
lingering fatigue or joint pain after COVID isn’t just stress, but actually a signal that
your immune system is attacking you? This is not a conspiracy theory. It is happening.
And science is now catching up with what many patients have been feeling all along. In the
last few years, I have evaluated quite a number of patients who develop autoimmune diseases
after recovering from COVID 19. But why is this happening and what are those warning signs?
In this video, I will discuss all of these early signs and will teach you what you need to do if
you develop those because if you catch this early, you may avoid years of suffering. I am Dr. Diana
Gernita, a boardcertified rheumatologist with over 20 years of clinical and research experience,
which diagnoses and treats patients with autoimmune diseases every day. Since the pandemic
began, you most likely heard of long COVID, respiratory damage, debilitating fatigue,
blood clots, but there is a darker, less known consequence, and those are the autoimmune
diseases. More and more people are now diagnosed with autoimmune diseases like lupus, rheumatoid
arthritis, shogran syndrome, multiple sclerosis, type 1 diabetes or guambare syndrome. If you
have a family history of an autoimmune disease, then your risk is higher. But even in people
without a family history of an autoimmune disease, I have diagnosed them with these conditions
after COVID 19. And the first question that comes to mind is how COVID 19 can cause or
trigger autoimmune diseases. Let’s think about this. COVID 19 and autoimmune diseases
have something critical in common. They can cause a ton of inflammation. Actually, they both
can cause wild inflammation. In both situations, your immune system launches a fullblown attack.
But instead of fighting the virus, your immune system cells can become confused at some point and
start attack your own body. In severe coid9 cases, there was a cytoine storm reported an explosion
of inflammatory chemicals like IL is 6,1 17 or 18. And these storms mirrors what the immune system
is happening or is doing that chaos that we see in autoimmune diseases. Plus some patients with COVID
19 develop a lot of antibodies auto antibodies like ANA, double stranded DNA, SSA, SSB and these
are the same auto antibodies that we see in people with lupus with rheumatoid arthritis or even in
people with antifphospholipid syndrome since 2020 when researchers from Stamford University told us
that about 50% of the people with COVID develop auto antibodies. We found out about more and more
studies that will say so. Is that a coincidence? Most likely it’s not because the presence or
persistent of these auto antibodies can announce that an autoimmune disease is going to happen.
And in 2022, we had the first studies that drew the attention that COVID 19 can increase the
risk of developing autoimmune disease. And this is the study that actually showed an increased
risk to develop lupus, rheumatoid arthritis, shograns disease, multiple sclerosis or diabetes.
And a newer study in 2024 again confirmed that autoimmune diseases or autoimmune inflammatory
rheumatic diseases may occur after the infection with COVID 19. And another study in nature also
brings attention on this subject. But what are the warning signs that you might develop an autoimmune
disease? If you had COVID 19, you know that fatigue is one of the most debilitating symptoms
that you can develop after this virus infection. And I had so many patients that I have seen
in the last 5 years that will struggle with fatigue that impairs their life for many months
or even years. It didn’t matter what they did, how much they sleep or even what supplements they
took because they remain exhausted. And although we don’t understand the reasons why these people
with CO 19 develop fatigue in some cases fatigue is a sign of inflammation or ongoing inflammation
and many autoimmune diseases can cause fatigue. Actually people with lupus with rheumatoid
arthritis with shogran can also have severe and disabling fatigue. So in my opinion, it might
be wise to check with an autoimmune specialist if that fatigue might be a sign of something that
is not necessarily related at this point with the COVID infection. Then many patients that had COVID
19 infection developed rashes, rashes on the skin, like the face or rashes on the legs. If the rash
looks like a butterfly on the nose or the cheeks, it could be because you might have developed
lupus. If the rash is very sensitive when you get outside in the sun and you develop severe
burning, which we call photosensitivity, again, it might be because of lupus. But patients with
COVID can also develop other kinds of rashes like pinpoint rashes that could be a sign of vasculitis
which is an inflammation of the vessels and there are many types of vasculitis depending on
what type of vessel is involved. However, some patients develop blood clots in the legs
or the lungs. And research showed that some people with COVID 19 develop anti-phospholipid
syndrome which is an autoimmune disease that can occur together with lupus or independent of
this disease. APL or antifphospholipid syndrome makes people more susceptible to develop blood
clots and it can cause a lot of other issues from changes in the skin appearance that can look
like a lace and we call this levido reticularis or it can lead to blood clots in the legs in
the lungs or even ulcerations of the fingers or the toes because these blood clots will stop
the blood flow of those vessels and will create complic applications. In my practice, I had many
patients who after COVID 19 infection developed joint pain. Now, let me tell you the story of
one of my patients. Elena was 29 years old. 3 months before she came to my office, she had
a severe case of COVID. She was very sick for about two weeks with lots of fever with cough
and malaise. She recovered after the COVID, but she remained extremely fatigued. And then in
about three months she noticed that she had pain in her small joints of her hands. And then in
a few weeks she developed pain in both of her wrist and the shoulders. Every morning she was
not able to remove her rings and her fingers were very swollen and they look like sausages. She
noticed a lot of morning stiffness that will last for a few hours. But as the day will go by, she
would have less stiffness and her hands will feel slightly better. She was seen by her primary care
physician who gave her ibuprofen, but that did not touch the pain. She was researching her symptoms
on the internet and she found out that there are a few cases of people with similar symptoms who
were diagnosed with an autoimmune disease. Then what did she do? She decided to bypass her
PCP advice and she came to see me. And after listening to her story, I order more specific
tests. And guess what? I have diagnosed Elena with rheumatoid arthritis. Is this a surprise
for me today? Not anymore. Because studies like this one are showing that people with COVID 19 can
develop rheumatoid arthritis, which is one of the most common diseases that I treat in my practice.
rheumatologist on call. Now, let me tell you about other possible autoimmune diseases. Have you heard
about Shogun’s disease? This is another autoimmune disease that I diagnose and treat in my practice.
And most people think about Shogran disease when they hear patients complaining about dry eyes
and dry mouth. However, in patients who suffer from COVID 19, Shograns disease can develop and
can look so much different. These patients can develop severe fatigue, brain fog, cognitive
issues, headaches, and a lot of symptoms of dysotonomia or neuropathy. Have you ever had
your heart start racing while you are sitting still and then you stand up and you feel dizzy or
you even faint? Your hands and your feet get icy, cold and then you suddenly feel short of breath
without any explanation. This can be more than just stress or anxiety. You might be dealing with
something that we call dysotonomia. And dysonia, it’s a malfunction of your autonomic nervous
system. And that’s a part of your nervous system that controls everything that you don’t think
about. Your heartbeat, your blood pressure, your digestion, and even your body temperature.
And in those people with dysotonomia, this automatic system starts misfiring. It’s like a
faulty electric panel controlling your body vitals function and that is flipping the wrong switches
at the wrong time. Some people develop what we call postural orthostatic tachicardia syndrome
or pots. And this is a common form of dysotonomia where your heart rate just jumps abnormally when
you stand up. other will feel completely wiped out and they could develop dizziness. And guess what?
After COVID 19, I have seen a massive increase in dysotonomia cases and some of these cases were
actually new cases of shogun’s disease that I diagnosed. Now, let’s talk about neuropathy.
Neuropathy means nerve damage. And it can happen when your immune system either triggered by an
infection or inflammation or autoimmune diseases, they start attacking your nerves. And this can
lead to burning and tingling in your hands and feet, numbness or shooting pain or loss of
coordination. And in some cases even bladder or bowel issues. And there are many types of
neuropathy, but one particularly important is the small fiber neuropathy which can affect the
tiny nerves that control the pain, the temperature and even automatic functions like the heart rate
or sweating. And many of my patients with Shogun’s disease developed that after COVID. They presented
to me with small fiber neuropathy. Some of these people develop neuropathy after receiving the
vaccine. But I will talk about that more in another video. When I talk about neuropathy, let
me tell you that there are some newer studies like this one that show that some patients also develop
muscle weakness and visual changes or visual loss. They were later diagnosed with multiple sclerosis.
And if you do develop these symptoms, it is better to see a neurologist, not a rheumatologist, a
neurologist. Now, have you develop any strange neurological symptoms and in joint pain, any
fatigue or brain fog after COVID 19? This could be signs of autoimmune activations. And here
at rheumatologist on call, we have diagnosed many patients with autoimmune diseases because we
offer a comprehensive assessment. We don’t ignore your symptoms. We don’t believe that they are in
your head. And especially if you have a family history of autoimmune disease, yes, you could be
at risk. And if you develop an autoimmune disease, the best thing to do is to be evaluated by an
autoimmune expert, someone like me, who will be able to recognize these early signs, to run
the appropriate test and treat you appropriately because I have seen many patients misdiagnosed and
mistreated for the last 5 years. And the truth is that COVID 19 may have forever changed how we
think about autoimmune diseases. If you wait until symptoms are full-blown, it may be too late
to prevent damage. And now that you understand how COVID 19 may trigger an autoimmune disease,
what about vaccines? Can the COVID 19 vaccine also unmask or protect you from autoimmunity? And
you need to know this. So, watch this next video.

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Introduction
Hi, this is Peter from Anatomy Zone. This video is the first in a new series we’ll be producing on clinical conditions and their anatomical and pathological coralates. We will be taking a look in this video at the structure of the corona virus responsible for the current pandemic and how its structure causes its clinical manifestation. Corona viruses are a large family of common viruses which are found in humans and animals. Many cases of the common cold are due to a corona virus. They have caused two largecale outbreaks in the past two decades. The SARS virus in 2002 and the MS virus in 2012. It’s generally been considered that these corona viruses could cause future disease outbreaks because they’re known to be able to evolve within animals and then jump to humans via an intermediate host. In SARS, palm civets and raccoon dogs were identified as the intermediate. Co 19 is an example of this which is believed to have jumped from bats to panggalins to humans in a local seafood market in Wuhan, China during 2019. COVID 19 refers to the corona virus infectious disease found in 2019. The actual disease itself is referred to as COVID 19, but the virus is called the SARS COV 2, which stands for severe acute respiratory syndrome corona virus 2 and was named because its structure very closely resembles that of the SARS virus from 2002. This is the seventh known corona virus to infect humans. Two of which was similarly highly pathogenic, MS and SARS. The other four are of low pathogenicity and endemic in humans.

Structural Overview of SARS COV 2
Let’s now take a look at the structure of the SARS COV 2 virus. So looking at this virus, we can see that it has a series of protein spikes on its surface which when viewed under a microscope appear like a crown which gives rise to the name corona which is Latin for crown and is therefore common to all the corona viruses. There are four structural proteins which is similar to other corona viruses. The S, the E, the M and the N proteins. The S stands for spike, the E stands for envelope, the M stands for membrane, and the N stands for nucleioapsid.

Spike (S) Protein and ACE2 Binding
So let’s take a look at these different structural proteins in turn. Beginning with this crown-like structure, which is the S or spike protein. This protein is responsible for allowing the virus to attach to the membrane of the host cell. It contains a receptor binding domain which recognizes a specific receptor, the angotensin converting enzyme receptor 2 which is expressed in the lungs, heart, kidneys and intestines. It has been shown that this protein binds to the ACE2 receptor with at least the same affinity and potentially as much as 20 times greater affinity than the SARS virus. This could be one of the explanations for the reasons why it’s spreading so easily. The spike protein itself has two functional subunits. S1 binds to the host cell receptor and S2 mediates the fusion of the viral and cellular membranes. Because of the critical role this protein plays in binding to target cells and cellular entry, it is a particular focus in the design of vaccinations and medical treatments for COVID 19.

Membrane (M) Protein
Let’s take a look at the next protein, the M or membrane protein. The membrane protein is the most abundant on the viral surface and defines the shape of the viral envelope. It can be thought of as the central organizer for corona virus assembly and interacts with the other structural proteins.

Envelope (E) Protein
Moving on to the E or envelope protein. This is the smallest of the major structural proteins on the viral membrane which appears to have several roles. We know that it is integral in the assembly and release of the virus from host cells and during viral replication it is largely localized at the site of intracellular trafficking. more specifically at the endopplasmic reticulum and the golgi apparatus. So essentially the M and E proteins play a critical role in turning the host cell apparatus into workshops where the virus and our own cells work together to make new viral particles.

Viral Envelope, Capsid, and Nucleocapsid (N) Protein
Underneath the surface proteins we have the viral envelope. This is the virus’s outer layer that is derived from the host’s cell membrane. So ourselves or the animals. It’s a fatty layer and worth noting that in contact with soap, it will break down, killing the virus. And this is the reason why handwashing with soap is so important to prevent the spread of this virus. Underneath this layer is what’s called the capsid. This is a protein shell that encloses the genetic material of the virus. Inside this capsid, we have the nucleo capsid or N protein. This protein is bound to the virus’s single strand of RNA, which is where all its genetic information is held to allow itself to replicate. The N protein appears to be multifunctional. In particular, it essentially inhibits a lot of the host cells defense mechanisms and assists the viral RNA in replicating itself and therefore in creating new viral particles.

Pathogenesis Foundations and Similarities to SARS
So we’ve looked now at some of the important structural features of the SARS Corona virus 2. A lot of our understanding of the pathogenesis of CO 19 comes from work on the original SARS virus. Because the viral structures and morphology are so similar, there is likely to be significant crossover in the biochemical interactions and pathogenesis.

Transmission and Early Infection
Let’s now look a little more at how the virus infects humans. So the virus is spread mainly by respiratory droplets, i.e. a cough or sneeze, which aerosolizes the virus, allowing it to travel into our nasal or oral cavities. We also know that it can live on surfaces for hours and even up to a few days on some surfaces. So, if you touch an infected surface, it’s very easy to then touch your own face and inoculate the mucous membranes in your eyes, mouth, or nose with the virus. Initially, it can get into the upper airway, so the nasal or throat area. And this is why you can get those symptoms like a common cold, stuffy nose, headache, sore throat, and fever. It is within the mucosal epithelium of the upper respiratory tract where primary viral replication is thought to occur. Similar to SARS, SARS corona virus 2 is able to get further into our respiratory system and into our lung epithelial cells where further viral replication occurs.

ACE2 Interaction and Cellular Entry
Let’s talk a little bit more about the ACE2 receptor interaction. The SARS corona virus 2 binds via its spike or S protein to the A2 receptor. This mechanism of binding is the same way that the SARS virus was able to bind to airway epithelial cells. The host cell has proteasis which are enzymes that break down proteins and these cleave the spike protein. We think that this process activates the protein in order to trigger the process of membrane fusion before injecting the viral genome into the host cell. A similar mechanism of protein cleaving facilitates cell entry in influenza as well as this mechanism of direct cellular entry. The virus may also enter the cell via endoccytosis. This is the process by which material enters a cell after being surrounded by an area of the cell membrane which then buds off inside the cell to form a vicle. Once inside the cell, virus specific RNA and proteins are synthesized within the cytoplasm. Further viral proteins are then assembled with the blueprint of information contained within the viral RNA using the host’s cellular machinery specifically the endopplasmic reticulum and golgi apparatus with specific processes to form the envelope glyoproteins. New virons are then assembled by fusing to the plasma membranes and released as vicles via the cellular exocitic secretary processes.

Inflammation, Symptoms, and Cough Mechanism
So the stresses placed on our own cells by viral infection and the interaction of our own immune system with the viral antigens presented by the infected host cells lead to cell death. During this process of cell death, multiple inflammatory mediators are released which creates an inflammatory response leading to a buildup of mucus and thickening and hyperplasia of the cells within our airways. This inflammation causes irritation of the cells lining our airways which leads to the cough.

Lower Respiratory Tract and Alveolar Impact
Let’s move further down into the lower respiratory tract now and see how the virus acts within the lungs. So to get there, let’s take a look at the path that the virus might take. So looking at the track here or the wind pipe, this branches into left and right main bronchi. These bronchi branch into lowbar bronchi. We have three on the right and two on the left. And these then branch into segmental bronchi. The segmental bronchi branch into bronchioles which terminate as respiratory bronchioles at the end of which are the alvoli. The alvoli are the tiny airfield pockets responsible for gas exchange. We have around 600 million of these alvoli and they are responsible for exchanging oxygen and carbon dioxide between the blood and the air we breathe in. Due to the direct action of the virus and also due to our own immune systems response to viral infection, the alvola walls can become inflamed and thickened and fill the alvolus with fluid which can impair their ability to exchange gases and this can lead to the symptom of shortness of breath.

Cytokine Storm and ARDS
In some people, this process of cellular infection by the SARS COV 2 virus can lead to an exaggerated immune response with a huge release of pro-inflammatory mediators causing what is known as a cytoine storm or cytoine release syndrome. Cytoines are small proteins involved in cell signaling and are crucial in mediating immune responses. This cascade of inflammatory mediators causes an uncontrolled systemic inflammatory response which leads to acute respiratory distress syndrome or ARDS. This is the rapid and widespread inflammation in the lungs which causes the epithelial and endothelial cells of the lungs to secrete inflammatory mediators which fill the alvoli. In addition, these inflammatory signaling cells recruit other cells of the immune system into the alvoli which further contributes to and amplifies the problem. Further, the systemic inflammatory state causes increased capillary permeability which results in even more fluid entering the alvoli. So essentially this is non-cardiogenic pulmonary edema compounding the problem. Overall, this pathological process severely impairs the ability of the lungs to exchange oxygen and carbon dioxide as it’s now become filled with fluid and inflammatory infiltrate. In cases of severe ARDS, invasive mechanical ventilation is required to adequately oxygenate the body. So that’s what underpins the pathology at the extreme end of the spectrum. In the large majority of cases of COVID 19 infection, the disease follows a mild course as the virus is eliminated via normal immune processes.

Imaging Findings
We will finish by taking a brief look at typical imaging findings. A chest radioraph may be normal in early disease, but when findings are present, we’ll typically demonstrate bilateral, peripheral, and basil airspace opacities. Plural eusions are rarely seen in COVID 19 infection. On CT as seen on these axial and coronal slices, typical findings are lower lobe predominant bilateral subplural ground glass density opacities. While these findings are frequently seen in COVID positive patients, these are not specific. The differential for these appearances includes other viral pneumonas, interstitial lung diseases such as cryptogenic organizing pneumonia and atypical bacterial pneumonas.

Conclusion
So that completes this video on the structure and pathogenesis of the SARS COV 2 virus.

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hello my name is Dr Lee I’m the chief of division of thoracic surgery and uh surgical director of the thoracic oncology program today I’d like to discuss with you uh uh about the treatment of early stage lung cancer lung cancer is an epidemic worldwide there’s approximately 1.8 million patients that are diagnosed with new lung cancer um equally almost equally there were uh 1.6 million patient deaths attributed to uh lung cancer in the United States we have an incidence of 224,000 patients that were diagnosed in 2011 and that’s our most recent data is is 2011 and uh almost equivalently there was uh 15 59,000 patients that develop uh a mortality related to lung cancer uh based on the International Association uh uh the iaslc for lung cancer uh there’s a retrospective data uh base that’s collected and in that registry uh OC carcinoma was the most common type of uh lung cancer uh it accounted for uh 43% of of non-s small cell lung cancer the second most common non-s small cell lung cancer is Squam cell and it compris of about 25% uh a minority of lung cancers are what’s called small cell type which is which is which makes up about 8% of uh lung cancer types so the two major types are non-s small cell and then small cell lung cancer type and several uh uh less common uh types of lung cancers with variable uh prognosis uh but most patients will be diagnosed with adnoc carcinoma or siso carcinoma lung cancer will present with uh symptoms that are fairly non-specific uh based on uh previous studies uh evaluating 3,500 patients that presented with lung cancer the most common types of uh symptoms they presented with uh included uh coughing uh weight loss dmia or shortness of breath uh chest pain uh hemoptisis which is coughing up of blood bone pain and horseness of Voice or change in the voice these were the most common types of symptoms that were uh that patients presented with often those symptoms will will precipitate studies and work up uh additionally uh important are uh risk factors for lung cancer um the most common cause of lung cancer is uh related to smoking 90% of lung cancers are linked to smoking there’s approximately a 15 to 30% more uh likelihood of developing lung cancer compared to non-smoker uh control patients uh smoking has a a cigarette smoke has approximately 7,000 chemicals 70 of which have been uh shown to cause cancer in in humans and in animal studies uh there’s an increasing number of patients with secondhand smoke exposure that die from uh lung cancer uh 7,300 patients will die every year uh secondary to U secondhand smoke exposure these are often family members that are exposed uh growing up or uh radon which is an inert uh gas you can’t smell it you can’t see it uh it’s a ra rown gas percolates from the ground up um it causes 20,000 cases of lung cancer each year uh the Environmental Protection Agency estimates that one in 15 homes in the United States will have high radon levels um other substances that have been associated with uh lung cancer uh include some of these that are listed here most commonly asbestos exposure uh and these have been shown to increase the risk of lung cancer personal and family history of lung cancer there’s increasing uh uh studies that uh attribute lung cancer to genetic uh uh relationships uh so uh family history is playing more of a role in uh patients that are at risk for lung cancer patients that have had radiation therapy to the chest in the past often these are patients that are cancer survivors from breast cancer or or lymphoma and they receive radiation to the chest as part of their treatment these are cancer survivors but later on in life they develop uh lung cancer because of the uh uh EXP exposure of the lung to the radiation that they received in the past uh there’s increasing studies that relate diet to lung cancer development um most notably smokers that take beta katene supplements have been shown to have increased incidents of lung cancer arsenic which is a chemical found in drinking water has been attributed to uh uh related to uh increased risk for lung cancer development so the combination of of of symptoms and risk factors will often prompt work up in additional studies to look for what is causing the patient’s symptoms or when there’s a concern for development of lung cancer uh signs and symptoms that we covered will often precipitate either a chest x-ray or a CT scan to begin with uh risk factors and asymptomatic patients uh can precipitate a screening uh CT scan a lowd do a chest CT scan uh to look for uh lung nodules and lung cancer …

Staging and Spread of Lung Cancer
… based on these studies understanding the the staging system is critical to how we interpret these radiographic exams and also how treatment is tailored for patients with lung cancer … Physicians talk about tnm staging … cancer can spread through the tissue itself within the lung … lung cancer can spread to lymph nodes … and when cancer spreads beyond the chest and goes systemically … most commonly the brain the liver the adrenal gland and Bone … so the extent of the tumor spread is what determines the patient’s stage and defines the tnm staging …

Imaging and Diagnostic Workup
… most commonly to figure out if it’s spread … we utilize these two scans a whole body pet C scan or a or a head MRI brain MRI … this is a uh picture of a uh fused petct scan … and this area that lights up is a lymph node … this picture here on the PET CT scan shows the actual lung cancer within the right lung itself … however uh the brain MRI is really what’s utilized to see if there’s any spread to the brain itself …

Surgical and Invasive Staging
… the surgical staging or the more invasive staging … clinicians uh think of the chest as … the mediastinum … accurate staging of these lymph nodes can be performed by indor bronchial ultrasound and oscopy ultrasound … we call this an Indo Broncho ultrasound … the oscopy ultrasound goes down the esophagus … the surgical uh approach to it is to make a small incision … a combination of either or both both are used to accurately bi uh stage the patients … and this really guides treatment …

Surgical Treatment Options
… lung cancer surgery … most of the time at UCLA we will perform the lung surgery using minimally invasive techniques called videy thoracic surgery or Vats … our ideal operation is to do a lobectomy … there’s two loes on the left side three loes on the right side … we make small incisions usually three … we use a camera scope to go in and we take part of the lung out and the lymph nodes … the minimally invasive approach has an uh is associated with earlier recovery and less pain … our discharge mortality and 30-day mortality at UCLA … compared to the national … averages …

Extent of Resection and Evidence
… lung cancer surgery … the amount of lung that actually comes out depends on … location and the extent of the tumor … ideally lobectomy is our standard operation but … we will take less than a lobe … wedge reection or a segmentectomy … in some instances … an entire right lung can be taken out … pneumectomy … reasons for ideally doing a lobectomy … based on a very Hallmark study … lung cancer study group … showed that there was higher risk of recurrence … but there are instances where it’s appropriate to do less than a lobectomy … edoc carcinoma in citu … patients that can’t tolerate ectomy …

Non-Surgical Local Therapies
… in early stage lung cancer … there are patients that simply don’t want to have surgery … in these individuals there are other local options … radio frequency oblation or cryo oblation … energy … generates heat … cry oblation … freeze the tumor … non-operative local treatments … my colleagues in radiation oncology … sterotactic body radiation therapy or sbrt … radiation beams that come in from multiple different directions … provides greater delivery … over a shorter course of treatments … ideal for small tumors … these non-operative approaches … are are great to to treat …

Transition to Advanced Disease Management
… thank you very much for for your time … my colleague … Dr … Goldman will be speaking to you about late stage lung cancer treatment …

Overview of Metastatic Disease Treatment
… my name is Dr Jonathan Goldman … I wanted to speak to you today about our treatment mostly … for widespread disease or metastatic disease … incredible development in the last five years … innumerable clinical trials … start out by discussing chemotherapy … then … targeted therapy … then talk about immune therapy …

Small Cell Lung Cancer Overview
… small cell lung cancer … highly tobacco related … very aggressive … surgery is is used rarely … focus … chemotherapy and sometimes radiation … targeted drugs called Notch Inhibitors … parp Inhibitors … immunotherapy is also being looked at …

Non–Small Cell Lung Cancer: Early vs Late
… non-s small cellon cancer … split it up into early stage … and later stage … role for chemotherapy particularly after … surgery for stage two and stage three … we mostly get involved for stage four … most commonly the brain bone liver and adrenal glands …

Modern Chemotherapy Approaches
… modern chemotherapy has become a lot better … anti-nausea medicines … pemetrexed … biologic drugs bism AB … maintenance therapy … several years of … ongoing cancer control … chemotherapy is still the main stay …

Treatment Pathways by Histology
… reviewing our general therapies for nonis mostly adoc carcinoma … pemetrexed … or a three drug combination carop platin petx and bevic ISM app … for second line or later … in sis cell … gem cabine … or … a taxing treatment …

Targeted Therapies and Driver Mutations
… revolution … mutations develop … identify that and block it … dramatic shrinkage … oral drugs … egfr Inhibitors … Tara and gilotrif or erot nib and a fat nib … Al Inhibitors … new generation egfr and ALK Inhibitors … other … Ross one … kras … Rett fgfr … proteins … like a satellite dish … drugs bind to that protein …

Evidence for EGFR and ALK Inhibitors
… important Trials … patients who had egfr mutations … more than 70% … benefited more from the egfr inhibitor … without egfr mutations … minimal benefit … ALK translocations … oral drug called cotb or Zori … major shrinkage … waterfall plot …

Resistance and Next-Generation Inhibitors
… next problem … treated with Tara … after four months … two years later … started to come back … why did the cancer become resistant … t790m … a long arm … gate has closed … smaller drugs that get around that gate … again seeing major response rates … UCLA played a really important part …

Immunotherapy and Checkpoint Inhibitors
… IM mapy … transformed the way we think about lung cancer … pd1 or pdl1 Inhibitors … encouraging the immune system … portion of patients get a major benefit … seems to last a long time … developing new strategies … checkpoint Inhibitors … cancer cells … cloaking system … allow the immune system to fight the tumor … tumors seem to grow … inflammation … those tumors May nearly disappear …

Q&A: Prognosis and Surgical Considerations
… how effective is lung surgery … prognosis … very much stage dependent … complete reection … margin negativity … lymph node status … defines whether patients should get chemotherapy … or if at all … earliest stage … fiveyear survivals … about 80 80% …

Preparing for Lung Surgery
… what should I think about if I have … lung surgery … is it appropriate for local therapy … accurate staging … assessing the risk profile … heart lung studies … cardiac studies … board certified thoracic surgeon … expertise in both minimally invasive … and … open techniques … high volume Center …

Recurrence Patterns and Multimodality Care
… other things that contribute to … long-term … survival … additional therapies … radiation … systemic therapy … stage … risk for … recurrence … locally … distant recurrence … multimodality treatment … most … Who present in an early early stage will not need those other treatments …

Chemotherapy’s Role and Patient Goals
… alternative treat treatment … be very careful … safety … appropriate option … will chemotherapy take care of the cancer … depends on the stage … prevent a cancer from coming back … where the cancer has spread … usually not able to take care of the cancer forever … treatment … important role … feel better and generally live longer … keep both quality of life and length of life in mind … exciting … new therapies … well tolerated … getting back to the things in their life … thanks very [Music] much

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hey everyone it’s s with register nurse rn.com and in this video I’m going to be going over part two of heart failure this video is part of a Cardiovascular inlex Review series that I’m going to be covering and in the previous video I covered part one of heart failure and I talked about the patho of heart failure the signs and symptoms the different types and things like that so if you haven’t watched that video be sure to check that out because that video builds upon this video and a card should be popping up so you can access that so what I’m going to do in this video is I’m going to be covering the nursing interventions and the medications given specifically in heart failure because that is really what the inlex exam and your nursing lecture exams like to hit on because as the nurse you need to know what your role is you need to know how to educate the patient and those common side side effects of those medications you’ll be giving in heart failure and then after you watch this lecture be sure to go to my website register nurse rn.com and take the free inlex quiz that will test you on heart failure and a card should be popping up so you can access that so let’s get started first let’s recap and talk about what is heart failure heart failure is where the heart is to weak to pump efficiently so it can’t properly give your body the cardiac output it needs to maintain the metabolic needs so you get some major issues going on and remember from the other video your left side of your heart or your right side of the heart can be affected or you can have both so remember with left-sided heart failure you’re going to get the pulmonary symptoms and with right sided heart failure you’re going to get those peripheral symptoms and the most common type of heart failure is left-sided and it can cause right-sided heart failure so keep those things in mind whenever we’re talking about medications and things like that so what are the nursing interventions let’s cover that first what is is your role as a nurse in a nutshell what you’re going to be doing is you’re going to be assessing that patient educating that patient and administering medications so first let’s talk about the assessing part what are you going to be doing okay as a nurse you were going to be assessing assessing their symptoms how are their symptoms are they presenting worse than before like if they’re in right-sided heart failure how is that peripheral swelling is it going down because chances are they’re going to be on medications are they responding appropriately to that or they getting worse um left side remember you get those pulmonary issues is the patient breathing better is there less crackles how are they doing with that next you’re going to be assessing the patient’s responsiveness to those medications medications such as digoxin you got to watch that heart rate because it can slow the heart rate down beta blockers things like that so you want to have them on continuous monitoring or be checking their Vital Signs often watching their blood pressure because they’re going to be on ACE inhibitors arbs or vasodilators and that really messes with the blood pressure and plus you’re shifting fluids out of the body they’re in fluid overload and you’re getting rid of fluids because they’re so they’re at risk for orthostatic hypotension and you’re going to be monitoring their volume status because we’re trying to diase them we’re trying to remove that fluid so they’re going to be on diuretics Chances Are The Physician will order fly catheter because a lot of times these patients come in they’re in fluid overload they’re going to be started on Ivy maybe Loop Diuretics like lasic it’s very strong diuretic especially going the intravenous route so they may need a foli to help drain all that urine that’s going to be coming out because getting up and going to the bathroom will wear them out because they’re already the respiratory system is already compromised and just going back and forth to the bathroom puts a lot of strain on them and you’re going to be monitoring assessing those daily weights every morning you’re going to get them up on a scale or use the bed scale and you want to monitor that weight because it’s very important how much weight they’re losing or possibly gaining then you’re going to monitor and look at those labs specifically you really want to watch potassium levels because a lot of the medications given in heart failure can cause hypo calmia or hyperemia for instance Lasix Lasix is a diuretic that wasts potassium so you really got got to monitor that lasx level um especially if they’re on dexin because if you have low potassium that can increase the chances of dexin toxicity hyperemia medications that can cause that that are sometimes prescribed in heart failure are like those potassium sparing diuretics that actually do the opposite of Loop Diuretics they keep potassium like alao and ACE inhibitors and arbs they can increase potassium so if you have a patient on an Ace inhibitor and aldactone are at Major risk for hyperemia so you have to tell the patient to watch their potassium intake also you’re going to be assessing and making sure they are following their cardiac diet and their fluid restriction diet a lot of patients have issues with this because um especially the fluid restriction diet normally they can only have about 2 liters of fluid a day so you have to constantly monitor what they’re having for breakfast for lunch and dinner and in between make sure they’re not cheating on that diet because we’re getting r of that extra fluid and we don’t want to just be putting it back in then we’re going to assess the edema in the legs that goes back to the patient’s responsiveness uh helping keep those legs elevated whenever they’re in bed will help promote returning that extra fluid back into the vascular system hopefully being excreted through the kidneys and keeping them in high fowers position to help with respiratory that position setting upright helps the lungs expand and helps decrease dispan next safety this is a big issue with your heart failure patients because number one chances are they’re going to be on some Vaso dilators or some other blood pressure medicine and um the body whenever they shift positions maybe lying in the bed they get up they can get really dizzy and they’re at risk for falling so you want to make sure you monitor them for that and the extra swelling and the legs and the feet make it really hard to walk and put the feet on the ground and it can lead to them falling okay now educating this is a big piece so remember this stuff write it down because as the nurse we want to educate our patients with heart failure and regardless if you’re not working on a cardiac unit maybe you’re going to work on Ortho your chances are you’re going to get patients with heart failure because this affects a lot of patients so our goal with educating is that we want to prevent readmission this disease process causes a lot of readmissions to the hospital and we want to prevent C um heart failure exacerbation so what you want to teach your patients is the following follow a low sodium diet guidelines are no more than two grams per day sometimes three so no more than two to three grams of sodium per day in your diet watch uh the hidden salts like in canned foods your sandwich meat your frozen meals things like that that you wouldn’t normally think have a lot of sodium in but do it in soft drinks next fluid restriction the doctor wants them on fluid restriction they need to make sure they monitor how much they drink a day because some of these medications can make you thirsty so um no more than two lers a day of fluid vaccinations make sure that they are they need to be aware that they need to get an annual flu vaccine and that they’re up to date on their pneumonia vaccine because illnesses can EXA exacerbate heart failure because it stresses the heart out when a patient gets sick next aerobic exercises that’s like your cardiovascular exercise they need to do light moderate exercise to keep that muscle nice and strong and do that as tolerated once their sympt symptoms start dissipating next daily weights it is so important that they weigh themselves every day because it is an early sign of CHS um heart failure exacerbation if they’re gaining weight so the guideline is if they’re weighing theirselves make sure they’re writing them down um they need to notify their doctor if they’re gaining any more than 2 to three pounds per day or 5 pounds per week that is signaling hey you’re starting to retain fluid something’s going on let’s go to the doctor um maybe they can prescribe some more diuretics so I don’t have to go to the hospital and readmit it so daily weight’s very important next compliance with medications a lot of times especially working as a nurse I have just seen where patients have quit taking their medicines maybe they couldn’t could afford their medicine so they quit taking them and this sent them into heart failure exacerbation so um very important they take those medicines next smoking sensation quits smoking very bad with the heart causes Vaso constriction hard on the heart and limiting alcohol consumption next um teach your patient those early signs and symptoms we just talked about the weight gain also if they notice that all of a sudden they can’t tolerate normal activities that they were doing like just getting up and going into the kitchen they notice that they’re starting to get a little short of breath or at night whenever they’re trying to sleep that they have to put a couple pillows behind them to sleep better which is called orthopedia those are some warning signs that hey I may be going into heart failure exacerbation now let’s look at the medications for heart failure when you’re studying these medications for the enclex or for your nursing lecture exams make sure you know the drug categories that are given in heart failure and what drugs are included in that category and how they work on the body the pharmacodynamics and their side effects and patient education very important key points you want to remember okay to help you remember the drug categories that are given in heart failure remember this pneumonic always administer drugs before a ventricle dies in heart failure our issue is with the ventricles they are either not pumping they’re not Contracting properly or they’re too stiff so they’re not filling properly so we want to make this heart work easier especially these ventricles so that pneumonic should help you remember those drugs that are included so the first a ACE inhibitors ACE inhibitors stands for Angiotensin converting enzyme and this is usually the first line of treatment in patients with heart failure and and it’s sometimes prescribed with a beta blocker which we’ll go over a little bit later these drugs tend to end in p iil and one example of a ace inhibitor is linil and how this drug works is that it blocks the conversion of an Angiotensin one to anot tensin 2 so you don’t have the conversion of anot tenson one going to anot tensin 2 and what does what how does that work well we know when ever Angiotensin 2 works it causes Vaso constriction but it’s not allowed to do that so in turn you’re going to get vasodilation which is going to decrease the heart the blood pressure and you’re going to get kidney excretion of sodium think back whenever Ang Angiotensin is being blocked what’s going to happen is it’s going to cause your aldosterone levels to decrease what does aldosterone do aldosterone whenever ever it’s being decreased it will cause your kidneys to keep potassium but excrete sodium which is what we want in heart failure we’re trying to get rid of all that extra sodium and fluid in the body and this strug is helping us get rid of that extra sodium however because it’s doing that it’s going to keep this H potassium but get rid of the sodium we have to watch out for side effects of hyperemia H potassium levels and for some reason with this drug these patients can develop a nagging dry cough and I have seen this as a nurse it’s for real and it really does happen they will literally cough every 3 to four minutes just this just over and over and over and it drives them crazy and it drives the people around them crazy so some people can’t tolerate this drug next drug arbs they if the patient cannot tolerate an Ace inhibitor they’ll be place on an ARB and how do arbs work ARB stands for angiotensin two receptor blockers so they’re a little bit similar so let’s look okay these like I said are used in place of ACE inhibitors they end in stin s a r t a n type of drug of this is low sartin and they work by blocking anot tensin 2 receptors so instead of blocking the conversion of angiotensin one anot tension 2 like the ACE inhibitors did this works by just blocking The receptors so again you’re going to get some Vaso dilation and it’s it’s going to have the same effects on the body as your ACE inhibitors because you’re going to have that decreased aldosterone and the patient’s going to keep potassium but excrete sodium however a side effect with this is hyperemia just like with ACE inhibitors but they will not get that dry hacking cough okay our other draw diuretics D these um either patient will be prescribed on Loop Diuretics or potassium sparing diuretics and these diuretics are used in a combination with these ACE inhibitors or an ARB they’re used together and um what your diuretics do is it helps your body get rid of that water and that sodium retention because in heart failure what we’re doing is retaining all this water we got edema everywhere retaining sodium so it helps us to excrete that decrease that edema and it helps the heart pump easier because it doesn’t have all that fluid volume in its Chambers trying to pump so it’s getting rid of that however a side effect of this is that this patient will urinate a lot so as a nurse you want to be monitoring that urine output very very closely and you want to monitor their bu and creatin and making sure we’re not diuresing them too much and putting too much strain on those kidneys okay an example of a Lube diuretic is Lasix remember with Lasix or Loop Diuretics they waste pottassium so before you get potassium I mean before you give Lasix check those potassium levels to make sure that they’re good because you go in and give some lasic and their pottassium levels already too you’re going to bottom that out even more so a lot of times Physicians will prescribe potassium supplements along with lasx and potassium sparing drugs drug alao um what these do they do the opposite of Loop Diuretics they keep um potassium so you have to watch out for um educate the patient not to consume foods that are high in potassium and to especially watch if your patient is on an ace or an R because remember they keep potassium and if they’re taking alaon you have a double risk of increasing that potassium level next beta blockers how do beta blockers work they work by blocking the nor epinephrine effects on the heart muscles so norepinephrine will naturally increase your heart rate so we’re going to block that from happening so beta blockers are going to slow down the heart rate they have a negative inotropic effect which increases my cardial contraction hence a fancy word for slowing the heart rate which will in turn decrease your heart’s workload because it is overworked in heart failure these drugs end in LOL typical ones used in heart failure are mopol carvol and bisol now typically the way that these beta blockers work they slow down your heart so they weaken the heart heart’s contraction so in some forms of heart failure especially acute heart failure that deals with systolic dysfunction you don’t initially want to use these beta blockers because let’s think back to the other lecture what is systolic ventricular dysfunction systolic that is the squeezing phase of the heart so there is an issue with this ventricle being able to squeeze that blood out so if we throw if this patient is an acute systolic dysfunction and we throw a beta blocker on them it’s going to weaken that heart contraction even more and we don’t want to do that because we have a contraction problem so it will sometimes the beta blockers will be used in stable systolic dysfunction and a lot of times these beta blockers are prescribed with ACE inhibitors or those arbs in combination now a lot of times beta blockers are used in disa diastolic dysfunction heart failure and what was ventricular diastolic dysfunction that was where remember di is the filling phase of the heart the resting phase and there’s an issue with the ventricle maybe it’s too stiff and it doesn’t fill properly with all that blood it needs to fill with but what a beta blocker can do is slow down that heart rate let that ventricle rest a little bit longer and fill more with blood so it can squeeze it out because it’s squeezing mechanisms gray it’s just the feeling so sometimes it will be used to treat um ventricular diastolic dys function now side effects of your beta blockers remember this um braa cardia so before you give a beta blocker check the heart rate make sure they’re not too braed cardic um it can mask hypoglycemic signs and symptoms in diabetics a lot of times a diabetic knows when their sugar is low because they may get Tac cardic hence you’re not going to get Tac cardic with brocard with beta blockers because it slows the heart rate down or they can get sweaty things like that and that mask those symptom so you need to teach your diabetics that and beta blockers can cause respiratory issues so it’s t they’re typically not prescribed especially the ones that aren’t selective for patients with COPD or asthma because it could cause Bronco constriction and um whenever the patients take these tell them not to take them with any type of juices especially grapefruit juice because it can interfere with your body’s absorption of the beta blockers okay next let’s look at a for anti-coagulant these are not used in every patient with heart failures so um typically it’s going to be used in heart failure patients who a lot of times heart failure and atrial fibrillation go hand in hand uh and you know with aib those Atrium are just quivering blood is pulling in there when blood pulls that’s not good because a clock can form can shoot through the heart and we can have an embolism so um if a patient’s in aib with heart failure they may be starting on an anti-coagulant or they have a history of blood clots or they have an ejection fraction less than 35% we talk about we talked about in the other video what ejection fraction was and um this is where your heart is not squeezing all that blood out properly so contraction isn’t good and if it’s not squeezing all that blood out that’s normally going in there with systolic dysfunction you’re going to have more blood pull in there so there’s a increased chance of developing a clot and shooting it through the heart okay next the for vasod dilators um a lot of times these are prescribed if a patient can’t tolerate an Ace inhibitor or an arm because it works by causing dilation and um One Drug which is an arterial dilator is hydrazine and it’s a lot of times sometimes prescribed with a nitrite called isroil and that is a Venus dilator hydrazine is is a specific drug that acts specifically on your um arteries and isoil is what acts on your veins so what happens is that you get dilation going on of those arteries and veins what how does this work how does it benefit the heart it decreases blood and fluid going back to the heart because the heart is already overloaded in heart failure with all this blood and all this fluid so we got all this nication going on and it will decrease the amount of fluid that’s going back and the workload that your heart has to undergo however side effects with this are hypotension because anytime you have dilation going on the patient is at risk for hypotension so you want to measure that blood pressure make sure it’s good before you get it and they are at risk for orthostatic hypotension so say your patients on these medications they’re laying in bed they need to get up to go to the bathroom you want to get them up slowly and gradually because they can get dizzy they can pass out and fall so you want to watch safety issues with that next D for de how does dexin work on the body I would remember this for sure okay it has a positive inotropic mechanism which means that it has that the heart has an increased ability to pump stronger however it has a negative chronotropic mechanism that allows it to beat slower so it’s a win-win it beats slower but it pumps more efficiently so this allows the heart to rest and P pump more blood which is great if you have left ventricular systolic dysfunction which is what this drug is sometimes used in however it’s not used as first line treatment for heart failure um it’s going to be used alongside with your ACE inhibitors or your diuretics because dexin can be a nasty drug it has toxicity issues and if a patient um has a low pottassium level goes into hypokalemia potassium level less than 3.5 they can go into into dexin toxicity so with this drug you want to monitor the drug levels um I would remember this a normal dexin level is .5 to two nanograms per milliliter this is where you want that patient to hang out anything higher than two is bad deox and toxicity and signs and symptoms of dit toxicity classic I have seen this this does happen um they’ll have nauseum vomiting and they’ll report some Vision change es uh they may all of a sudden start seeing some yellowish green Halos um they can be bra aaric as well and what would happen you notify the physician immediately don’t give another dose of dexin and um The Physician will probably order the antidote for dexin which is digine very easy to remember it tells you what it is digine d i g i b i n d matches dejin that is the antidote for that um whenever you are giving dexin as a you all always want to check the apical pulse and make sure it’s greater than 60 beats per minute before giving the dose okay so that is a review the part two review of heart failure be sure to go to my website register nurse rn.com and take that free quiz and thank you so much for watching and please consider subscribing to this YouTube channel