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ANEMIA — Transcript

by Telesalud Minsa Telecapacitaciones · 11,143 words · 1,760 segments · language en · Watch on YouTube

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0:01Full screen is displayed. There you go.
0:05Yes, now you are in screen mode.
0:08Now you can start. Correct.
0:10Correct, doctor. Go ahead.
0:12Well, with all due apologies for the
0:14delay, because we have had technical
0:16problems, unfortunately it could not be
0:18enabled in a timely manner. What we
0:21have to talk about this morning is what
0:23iron deficiency anemia is. The first of
0:26these is the most common worldwide. Oh,
0:30and the second is due to the morbidity
0:35it presents. As a general concept, what
0:40I want you to understand is why the
0:42management of anemia is so important:
0:44oxygen is important for metabolism and
0:46cellular respiration, and it is what
0:48hemoglobin transports that reaches the
0:50cells; it allows these cells to have
0:52the metabolism and cellular respiration
0:54that are useful for my body to function
0:56. Now, imagine that if you don't have a
1:02car and you don't have gasoline, how
1:03can you start it? It's a crude example,
1:07but so that you understand me, let's
1:08imagine the same thing, that oxygen
1:10doesn't reach the cells, how can the
1:12cells work and perform their functions?
1:15Let's imagine the cell of the central
1:17nervous system, the neurons that are so
1:19basic and important for cognitive
1:21development, right? Imagine that if
1:25they don't have oxygen, how could we
1:27have it in that little brain or that
1:29brain of that person? Therefore, it has
1:33repercussions. Uh, so the cognitive
1:38deficit, cognitive deficit in patients
1:40in vulnerable areas, let's call them,
1:42peripheral areas, the management of
1:44anemia is transcendent. Another crude
1:50example of this is that we say that one
1:52of the presidential candidates with
1:53their famous phrases is because he
1:55didn't have good neurological
1:56development due to deficit or because
1:58he had anemia. I think you understand
2:01who I'm referring to this morning. What
2:04I'm going to talk about are six points.
2:07Well, the main thing is to talk about
2:09the diagnostic basis, iron deficiency
2:11anemia itself, megaloblastic anemia,
2:13therapeutic management, education and
2:15follow-up, and specialized referral
2:17when there is already management for a
2:19specialist in the hospital. Please, if
2:24you have any questions or something
2:26that is not understood or that is not
2:28clear, do not hesitate to let me know,
2:30either with a direct question or in
2:31writing so that I can answer the
2:33question that I have. Right? Very good.
2:41The important thing about primary care
2:43is early diagnosis of anemia. We
2:46currently have complementary tests such
2:48as a blood count and it is easy to make
2:50a diagnosis of anemia. The diagnosis if
2:55it is anemia, iron deficiency anemia,
2:57can be done later, but the basic thing
2:59is that we make the diagnosis of anemia
3:01and with that we can prescribe
3:03treatment or refer the patient to a
3:05specialist and, uh, turn this off,
3:07please. and refer the patient to a
3:10specialist and therefore the
3:12appropriate management. Right? Very
3:14good. Let's see, regarding the
3:21epidemiological aspect, which is what
3:23we sometimes care about a little more,
3:25we can say, for example...oh, sorry, we
3:27can say, I told you at the beginning
3:29that iron deficiency anemia is of
3:31global importance, it is the most
3:33frequent at a global level, affecting
3:35millions of people and generating a
3:37significant impact on public health.
3:41Right? Megaloblastic anemia itself is
3:44not so frequent, it represents about 3%
3:47worldwide, but it is emerging, what is
3:49important are the diverse clinical
3:51implications that this deficit can
3:53generate. Right? Very good. Let's see.
3:57Ah, as general knowledge, let's see. Uh
4:02, we know that the populations in the
4:04Cajamarca regions, Huancavelica and Ica
4:06are, uh, the most prevalent in anemia.
4:12Ah, and there is also information that
4:14Ica is a prevalent area in terms of
4:16gestational anemia, as general
4:17knowledge. Uh, it should be emphasized
4:21that first-level health personnel are
4:23the fundamental pillar in the
4:24management of these conditions. They
4:27are the ones who make the early and
4:29timely diagnosis of anemia. And if the
4:32management is going to be simple, but
4:34if there is no response to this
4:35treatment, the most important thing is
4:37to make the referral. Finally, we are
4:41going to do some important part of the
4:42situations in which referrals are made
4:44to the specialty. Uh, to emphasize that
4:49there are 82 million people affected
4:51globally. I already told you that it is
4:53the leading cause of iron deficiency
4:55anemia worldwide. 91%, I emphasize,
4:57iron deficiency anemia and 97%of
4:59neurological manifestations associated
5:01with megaloblastic anemia or B12 and
5:03acid-phosphatidylcholine deficiency.
5:06Correct? Very well, let's continue then
5:08. Let's see, the initial algorithm for
5:11anemia in general, what would be step
5:13one? Uh, normally patients with anemia,
5:19either of the two, be it iron
5:20deficiency anemia or megaloblastic
5:22anemia, will generally present fatigue
5:24with moderate exertion. Moms or young
5:29women will say that when they walk one,
5:31two or three blocks they feel tired and
5:33need to rest to keep moving forward.
5:38The other thing is headaches or
5:39increased drowsiness, apart from the
5:41fact that we may see pale or yellowish
5:43skin in some cases when the anemia is
5:45severe. So, our first step in this case
5:49is a complete blood count, which is a
5:51universal test and is currently
5:53available nationwide. Step two,
5:56confirming anemia. Anemia, for
5:58practical purposes, below 11 is anemia.
6:02Below 11 is anemia. If you want to be
6:06theoretical and base yourself on the
6:09WHO, hemoglobin below 13 in men,
6:11hemoglobin below 12 for women is anemia
6:13. And in pregnant women or during
6:17pregnancy, hemoglobin below 11 is
6:19anemia. This is according to the WHO as
6:23a general knowledge, practical
6:24definition. In my case, based on daily
6:28practice, I say hemoglobin of 11 in any
6:30population is anemia. Step three is to
6:36evaluate the mean corpuscular volume or
6:38the mean electrocytic index, which is
6:39based on the value that is in it will
6:41define for me whether it is microcytic
6:43or macrocytic anemia. What does micro
6:47or macrocytic mean? That is, the cells
6:50are very small or the cells are very
6:52large, in this case, the erythrocytes.
6:56Remember that hemoglobin refers to the
6:58population of erythrocytes. So, when
7:02the erythrocytes, which are the
7:04hemoglobin cells, decrease or are very
7:06small in the bloodstream, it is called
7:08micro. And when it is very large it is
7:11called macro. As a kind of review of
7:16what anatomy is. Remember that the bone
7:20marrow produces or processes or forms
7:22three types of cells. Red blood cells
7:26that serve to transport hemoglobin.
7:30White blood cells that serve as my
7:32defense system, defending me from
7:33aggression, whether it be viruses,
7:36bacteria, parasites, etc. And finally,
7:38the platelets that allow or protect me
7:40from bleeding. If I have a wound, the
7:44platelets act and inhibit bleeding,
7:46therefore, I cannot hemorrhage. Here,
7:50if you look on this right side, it says
7:5280-90. If it is below 80, it is called
7:56microcytic anemia. The most likely
7:58cause is iron deficiency anemia, among
8:01others. Correct? If the BCM is greater
8:03than 100, it is called macrocytic. And
8:06why macrocytic? What happens is that in
8:10the bone marrow, the erythrocytes
8:11undergo maturation. In order to be able
8:15to enter the bloodstream and fulfill
8:17the function of transporting oxygen,
8:19they need an adequate size, between 80
8:21and 100 fetoliters. So, but when there
8:24is macrocytic or megaloblastic anemia
8:27or due to a deficiency of B12 or folic
8:29acid, these cells are produced properly
8:33, therefore they come out in an
8:35immature form. When cells are made,
8:41they start with large cells and mature
8:43until they become erythrocytes that
8:45have an average size of 80 to 100 ng/L.
8:50Since macrocytic anemia or a deficiency
8:53of B12 or folic acid does not allow for
8:55this timely maturation, they come out
8:57immature, they come out large, which is
8:59why they are called megaloblastic,
9:01megalo for large, and blastic for
9:03immature cells. And normoscytic anemia,
9:07when we have a normal BCM between 80
9:09and 100, this requires additional
9:11evaluation. Well, as a culture or as a
9:16product of this training, what is very
9:18clear is the BCM. If I have a BCM below
9:2480 ng/L, microcytic anemia, when I have
9:27a BCM or average red blood cell index
9:30above 100, it is called macrocytic. So
9:35far, any questions or concerns? To
9:45emphasize the hemoglobin thresholds
9:47according to the WHO, which we have
9:49already mentioned, in adults under 13
9:51anemia, in non-pregnant adult women
9:53under 12, anemia, and in pregnancy
9:55under 11, anemia. This concept should
10:02be clear in daily practice when
10:03hemoglobulin below 11 is found in any
10:06population, it is anemia. Therefore,
10:11the next part is to visualize the BCM
10:13that I already mentioned and how it
10:15should be interpreted. Well, let's go
10:20to our iron deficiency anemia, which is
10:22the most frequent, with a high
10:24morbidity index and future
10:25complications in neuronal development,
10:27if this continues, if iron deficiency
10:29anemia is not corrected. How do I
10:33define iron deficiency anemia? I define
10:35it as a condition resulting from a lack
10:37of iron that prevents the adequate
10:39production of hemoglobin. What is
10:41hemoglobin? Hemoglobin is a protein or
10:44molecule that has four emo groups and
10:46oxygen is transported within these four
10:49groups. And as I was telling you at the
10:52beginning of this talk, oxygen is
10:54predominant, important, really
10:59important in cellular respiration. If
11:02there is a lack of oxygen, my body does
11:04not work properly. I should emphasize
11:08that it is the most common anemia
11:10globally, worldwide. I have nothing
11:13more to mention here. It represents 25%
11:16of the world's population, right? It is
11:19more frequent in women, the elderly,
11:21and the pediatric population. Perhaps
11:23what I should highlight here is the
11:25following. Iron deficiency anemia can
11:29affect extreme populations, vulnerable
11:31populations, children, and the elderly.
11:35So, we must take care of these
11:36populations. What is the
11:39pathophysiological cascade? That is,
11:42the decrease in iron in the body. The
11:46decrease in iron occurs due to losses.
11:48So, remember, iron deficiency anemia is
11:51a loss. Loss in the body. How do I lose
11:54blood? In women of childbearing age,
12:00that is, in the process when they have
12:02monthly menstruation, if menstruation
12:04is abundant, whether in days or in
12:05bleeding, it will generate anemia in
12:07the long term. Right? That's one part.
12:15The other part is in adult males due to
12:17gastrointestinal loss. So, iron
12:21deficiency anemia, as a kind of
12:23conclusion, is blood loss. Blood loss.
12:28How do I lose blood? I already told you
12:32, in women of childbearing age due to
12:34menstruation and in men at least
12:35between 20 and older, it is
12:37gastrointestinal loss. The depression
12:41of reserves. I need to have ferritin,
12:48which is a protein, an acute phase
12:50reactant protein that originates in the
12:52liver and generates reserves; I must
12:54have plenty of iron, but remember: if I
12:56have continuous blood loss, this will
12:58decrease the decrease in transport, the
13:00decrease in transport, the iron is
13:02transported through transferrin. These
13:10are markers of anemia. When the
13:13ferritin level is below 30 microg per
13:15liter, it tells me that it is anemia.
13:18When the transferrin saturation is
13:21below 16%it is anemia. Here also to
13:25differentiate that in the English
13:27literature it is 16%, in the Spanish
13:29literature it is 25%. Well, so that you
13:35keep in mind, if I add 16 + 25 it would
13:38be 41/2 20%. As a Peruvian and follower
13:42of foreign biography, I consider 20%,
13:45but the theory says 16%. Defective
13:49erythropoiesis. Remember, if
13:54insufficient iron does not reach the
13:56bone marrow, there will be a deficiency
13:58in hemoglobin and therefore a
13:59deficiency in the formation of
14:01erythrocytes and, of course, a
14:02deficiency in hemoglobin and
14:04established anemia. We have already
14:09mentioned the parameters, correct? Here
14:11, just to reaffirm what I was saying,
14:26the most frequent cause of microcytic
14:28anemia, remember the BCM or mean
14:30ferritin index is less than 80, correct
14:32? And it requires confirmation of
14:36ferritin. Here there is also a concept
14:41that we will discuss later regarding
14:42ferritin and its value in diagnosing
14:44iron deficiency anemia. What I do need
14:50to do is make a differential diagnosis
14:52of what I have, microcytic anemia, and
14:54differentiate it from chronic disease
14:56and other causes of microcytosis. This
15:01usually occurs in children at an early
15:03age. Therefore, it is not common in our
15:08country for an adult to have thalamia,
15:10it is mostly in pediatric age. Now, if
15:15we take into account the influence of
15:17people who visit us, such as
15:18Venezuelans, there is a high incidence
15:20of thalamia in them. Therefore, this
15:25prevalence of thalamia is increasing,
15:27but in any case it is due to imported
15:30cases, not ours. So, an algorithm, a
15:36systematic diagnosis, which, suspected
15:38anemia, I already told you in the
15:40clinic, fatigue, paleness, among other
15:42things, a complete blood count plus BCM
15:45. And the BCM is less than 80,
15:48microcritical anemia. If the
15:52iron-deficiency ferritin is less than
15:5430 microg per liter, that confirms
15:56iron-deficiency anemia. Now, here comes
16:00a larger concept in which the current
16:02literature suggests that I should use
16:04PCR management. Why PCR? PCR is also an
16:11acute phase reactant that allows me to
16:13see if I have an inflammatory process
16:15in my body, an infectious process or a
16:17chronic disease. So, if this is below
16:23five, correct, I confirm this with
16:26ferritin. But if the PCR is greater
16:32than 5, then the validity of the
16:33ferritin less than 30 changes to a
16:35validity of less than 70 microg per
16:37liter. Do I make myself clear so far?
16:44Remember, microcytic anemia, acerbic
16:46perritin, if it is less than 30, but
16:48without conditions of, uh, inflammation
16:51, without conditions of, uh, chronic
16:53disease, without conditions of, uh,
16:55infection, then less than 30 mg per
16:58liter is valid. But if the CRP is
17:03greater than 5, then two additional
17:05parameters, ferritin, but no longer
17:07less than 30, but less than 70 mg per
17:09liter. and the percentage of
17:12transferrin saturation less than 16%.
17:16Correct? Well, as I told you, ferritin
17:20is the central biomarker for diagnosis
17:22as long as there is no infectious,
17:24inflammatory process or chronic disease
17:26. And to confirm anemia with an
17:32elevated CRP, I use transferrin
17:34saturation, which is a good marker.
17:39Very good. We already talked about
17:42ferritin, I told you that it is a
17:44protein produced in the liver that
17:45stores iron and its concentration is a
17:47reflection of the body's reserves of
17:49this metal. Just in case, so that we
17:53have a more general idea, it is the
17:55following. Iron stores in anemia drop
18:00to zero. So, the most important thing
18:03for me is not to improve hemoglobin,
18:05which can be improved in two to three
18:07weeks. The most important thing is iron
18:11stores in ferritin, and that lasts
18:13three to six months, minimum 3 months,
18:15minimum 3 months, maximum 6 months. So
18:19this is important for you to keep in
18:21mind. Since I already told you that its
18:26limitation is important, ferritin is
18:28even normal or elevated in inflammation
18:30, infection or chronic diseases. Let
18:34this remain as a concept, as a
18:36conclusion from this morning. Well, I
18:39already told you, the diagnostic
18:41thresholds are less than 30 when these
18:43three problems are not present, and
18:45less than 70 when these three problems
18:47are present, and where I use a CRP
18:49greater than 5 mg as an evaluation
18:51parameter. Oh, please, can you tell me
18:56if I'm going too fast? Am I okay? Can
18:59you hear everything? Aren't you telling
19:00me anything? Of course, doctor.
19:04Very good. Okay, to reaffirm the
19:07concept of ferritin and CRP, right?
19:11Ferritin, as I told you, is an acute
19:13phase reactant protein that increases
19:15in response to inflammation. Therefore,
19:18it will be elevated in inflammatory
19:20processes, infectious processes, or
19:22chronic diseases. Therefore, ferritin
19:26is not useful as a marker of iron
19:28deficiency anemia. Yes, you should have
19:32that. We have already discussed the
19:36double-test strategy for CRP, that is,
19:38I have ferritin and if I have an
19:40infectious process, a chronic disease
19:42process, I ask for CRP and if it is
19:44above five, then the new value is no
19:46longer 30, but 100 microg per liter. I
19:52also want to mention that depending on
19:54the laboratories in the hospital, we
19:56have a marker of 100 for ferritin just
19:58in case. Here it is 30 according to the
20:01biopsy. I already told you about the
20:05CRP plus simultaneous CRP to make the
20:07confirmatory diagnosis. If the CRP is
20:10less than CCO and there is no
20:12inflammation, infection or chronic
20:14inflammation, the ferritin marker is
20:16less than 30 microliters per liter. And
20:20if I have an inflammatory process,
20:22inflammation or chronic disease, the
20:24marker is no longer 30 but 70. Or in
20:27any case, if I have the possibility of
20:29transferrin saturation less than 13%, a
20:31functional indicator that it is iron
20:34deficiency anemia. Correct? These
20:39markers allow me to differentiate
20:41between iron deficiency anemia and
20:43chronic disease. Chronic disease can be
20:48established by the patient's history,
20:51for example, chronic renal failure,
20:53diabetes, autoimmune diseases such as
20:55lupus, rheumatoid arthritis, among
20:57other chronic diseases. Okay. As part
21:04of the anemia profile, what is
21:06requested is iron ceric, perritin,
21:08transferrin, vitamin B12 and coacid. In
21:13the hospital, we ask for reticulocytes,
21:16and hypothyroidism is closely
21:17associated with anemia. Therefore, you
21:21can also ask for THC and free T4 to
21:23even define megaloblastic anemia
21:25associated with hypothyroidism and
21:27anemia. Biochemical parameters,
21:34saturation, I already told you what the
21:36mean body volume differential count is.
21:41This is a parameter that is more
21:42commonly used in hospitals than in
21:44peripheral areas. Transferrin
21:46saturation less than 13 or 16%. Well, I
21:51told you that in the case of the
21:53hospital, we handle less than 20%and we
21:55obtain a more accurate and precise
21:57acquisition of what anemia is. What I
22:00do want to mention here is the finding
22:02of the blood protein, the peripheral
22:04lamina. You will see two
22:06characteristics associated with iron
22:08deficiency anemia, microcytosis and
22:10hypochromia. We have already defined
22:14microcytosis, which is a small or
22:16reduced erythrocyte with a BCM less
22:18than 80. And hypochromia are pale
22:20erythrocytes, lighter in color, but
22:23mostly they are pale. That is
22:26hypochromia, correct? Very good.
22:29Regarding anisocytosis, these two
22:35parameters, although they help me, are
22:37seen in many pathological entities,
22:39therefore it is not so much that having
22:41these two also increases the diagnosis
22:43of iron deficiency anemia. What is
22:47anisocytosis? Variability in the size
22:49of the cells. It means that, let's say
22:54that if I have a size of small, medium
22:56and large, in the anisocytosis I will
22:58find all three sizes in the
22:59erythrocytes, in the peripheral layer.
23:04And poicolocytosis means variability in
23:06shape. Remember that the cells have a
23:09biconga shape, but this here, for
23:11example, says: donut-shaped discs or
23:13folds of the efforth can be observed;
23:15that is more theoretical. But it will
23:19change in shape: the biconcave shape
23:21that an orytocyte like this one here
23:22normally has, like a kind of donut with
23:25a center, or rather, if you've ever
23:26seen a Mexican hat from above, this is
23:28a Mexican hat. That's the shape of a
23:32normal erythrocyte, but it will change
23:34in what is anemia. But I tell you that
23:37it is not necessarily associated with
23:39iron deficiency anemia. There are other
23:41entities that have it. Here I emphasize
23:44the value of the proteis; it is an
23:46economical and powerful tool that
23:48offers valuable clues about the nature
23:50of the anemia. What are you going to
23:52bet on? You will present microcytosis
23:54and hypochromia, correct? Very good.
24:00Here is a general diagnosis as well as
24:02a cultural diagnosis, let's say a
24:04differential diagnosis between what is
24:06iron deficiency anemia and thalacemia
24:08minor. I insist, thalacemia minor or
24:11thalacemia major, either of the two
24:13occurs mainly in the pediatric
24:15population and there is an important
24:17value in this sense, the antecedent.
24:21Thalacemia minor is passed from mother
24:23or father to child. Then there will be
24:25a history in this population, it is not
24:27that it comes out, it is not that it
24:29debuts out of nowhere, there is a
24:31hereditary history. Therefore, this
24:34information is available. As I said a
24:36while ago, it is a bit difficult for an
24:38adult patient to debut with thalassemia
24:40minor in Peru, that is, if they are
24:42Peruvian by birth. Now, if they are
24:44Peruvian by birth, but their parents or
24:46one of them is a foreigner from Europe,
24:48especially the Mediterranean, they are
24:50at high risk of developing this. The
24:54European or Mediterranean population
24:56tends to have a high frequency of
24:58developing this thalassemia. Regarding
25:02the parameters, iron deficiency anemia,
25:04we have already said that the average
25:06index is less than 80, in both it is
25:08less than 80, so in both I have
25:10microcytosis. The red cell distribution
25:14is elevated, here it is normal and the
25:16ferritin in what is iron deficiency
25:18anemia is less than 30, that is, it is
25:20decreased in what is normal or
25:22increased in thalassemia minor. That's
25:26what I would like them to have as a
25:27general culture, more than anything
25:29else, more than anything else, of
25:30representation, but I'll tell you again
25:32that this is very common in Peru. What
25:35we are going to look for is iron
25:36deficiency anemia, which is highly
25:38frequent in pediatric populations, in
25:40populations of older adults, and in
25:42women of childbearing age. Well, for
25:51anemia, for low-grade anemia, the
25:52standard is a hemoglobin test, which is
25:55already requested in the hospital or by
25:57the specialty. Megaloblastic anemia, as
26:04I was saying at the beginning, is an
26:06uncommon anemia, representing about 2
26:08to 3%, but it is important in terms of
26:10neuronal development or neuronal damage
26:12, which can lead to damage to neurons,
26:20demyalination, if it is not adequately
26:23controlled or treated in a timely
26:24manner. So, the importance of this
26:28morning is to make the diagnosis of
26:30megaloblastic anemia. The first part I
26:34told you, hemoglobin or blood count, a
26:36hemoglobin below 11 is anemia and if
26:38you are observant you go to BCM. If the
26:44BCM is less than 80, if it is higher, I
26:46suggest greater than 90. Here in theory
26:49it says 100, but I suggest greater than
26:5290. Regarding the pathophysiology, well
26:54, there are two vitamins that have to
27:01do with this type of anemia, B12
27:03deficiency or cholic acid deficiency.
27:06Where do I find these vitamins? Vitamin
27:11B12 is found mainly in red meats, eggs,
27:14milk, tuna, among others. Meat, animal
27:21meat, especially animal meat, correct.
27:24Chicken, turkey have it, but in a
27:25smaller percentage. I mainly find it in
27:29red meats, liver, pork, blood sausage,
27:31bofero, chanfainita, eggs and milk.
27:35Correct? Even in the outpatient clinic,
27:39I recommend that patients consume seven
27:41products a week: red meat, liver, pork
27:44belly, blood sausage, pork rinds, eggs,
27:46and milk. These certain products
27:51guarantee 80%of your hemoglobin. 80%of
27:54hemoglobin is provided by iron and B12.
27:59So, in my normal diet, I am guaranteed
28:01not to have anemia. And folic acid is
28:06provided by all green products, green
28:08leaves or peels, and any green
28:10vegetable will provide me with folic
28:12acid. And if B12 and iron account for
28:1880%, therefore, folic acid accounts for
28:2020%. Right? Both are important because
28:27they participate in DNA synthesis. This
28:31is the most important thing here.
28:35Vitamin B12, cobalamin, is an essential
28:37cofactor for DNA synthesis and myelin
28:40maintenance. If this decreases, it
28:44causes demyelination and therefore will
28:46create long-term sequelae if it is not
28:48treated promptly. So here it says
28:53deficiency causes hematological
28:55manifestations, as I already told you,
28:57anemia and neurological manifestations,
29:00demyelination. Oh, it would also be
29:03important to mention here that when B12
29:06is severely deficient, when the deficit
29:08is present for a long time, it can
29:09generate pancytopenia, a deficit in all
29:11three cells of the bone marrow. Folic
29:16acid is essential for the synthesis of
29:18nucleotides and amino acids. Its
29:20deficiency mainly affects rapidly
29:22dividing cells. Therefore, remember,
29:25B12 and folic acid participate in DNA
29:28synthesis, which is why they are
29:30important. Folic acid is especially
29:33important in pregnant women. Pregnant
29:37women who have anemia and a folic acid
29:39deficiency will have nerve damage or
29:44alteration or present with a virgin
29:46spine, just in case. That is important.
29:50That is why pregnant patients should be
29:51given folic acid in addition to iron.
29:54Or it is even recommended that folic
29:56acid should be started before getting
29:58pregnant, just in case. Well, I already
30:03told you, neurological manifestations,
30:05demyelination can generate subacute
30:07combined degeneration of the spinal
30:09cord. Look at all the risk that this
30:13deficit can generate, right? And above
30:16all, it can cause irreversible
30:17neurological damage. Irreversible if
30:20adequate treatment is not given. Uh,
30:23just to emphasize that I had already
30:25said it here, B12 and cholate
30:27deficiency compromises the synthesis of
30:29purines and pyrimidines, that is, it
30:31participates in DNA synthesis. Defect
30:35in DNA replication affects myeloid and
30:37retroid cells, that is, the cells that
30:39generate all the cellularity of the
30:41blood. Ineffective erythropoiesis. What
30:46does ineffective erythropoiesis mean?
30:48The accumulation of large immature red
30:50blood cells. How does that translate? I
30:52was telling you that red blood cells go
30:54through a maturation process from
30:56blasts to erythrocytes. It is a
30:59maturation process that, more or less,
31:01takes place in the marrow and the bone
31:03marrow. But I was telling you that
31:10these immature erythrocytes enter the
31:12bloodstream without the proper
31:14physiological maturation process and
31:16they come out large; that is why it is
31:18called erythroblastic and megaloblastic
31:20. So, these large cells with immature
31:27erythrocytes enter the bloodstream and
31:29because they are immature, they also
31:31cause destruction, just in case. There
31:36is a destruction of immature
31:37erythrocytes and that destruction can
31:39even generate an increase in velurubin,
31:41an increase in lactic kinase. It can be
31:46similar or masked as a type of
31:48autoimmune erythrocyte anemia, just in
31:50case. Macrocytic erythrocytosis or
32:01megaloblastic anemia, right? Let's
32:06continue. Causes of macrocytosis,
32:08differential diagnosis. That is also
32:11important that I want to mention. Hm.
32:15While it is true that the main cause of
32:17megaloblastic anemia is B2O deficiency,
32:19the most predominant and frequent cause
32:22. But there are also other causes, such
32:27as drug intoxication, moderate to
32:29severe hypothyroidism, liver failure,
32:31and chronic alcoholism. In other words,
32:36I should not just look up the blood
32:38count, the hemoglobin, and say anemia
32:40and a BCM greater than 100 is
32:42megaloblastic anemia. Epidemiology is
32:46important. If a patient takes five
32:50cluborasils methotrexate associated
32:52with sodium hypochlorite, hydrobromide,
32:54in the case of patients with HIV on
32:57HAART, they may have this B2 deficiency
32:59. It is common in the outpatient clinic
33:04to find B12 deficiency in patients with
33:11reactive HIV, correct? Or with a
33:14diagnosis of HB. Severe hypothyroidism,
33:17moderate to severe, as I have already
33:19told you, causes megaloblastic anemia.
33:22Liver failure, that is, liver cirrhosis
33:25also causes megaloblastic anemia and
33:27chronic alcoholism as a folate
33:29deficiency. Okay, so that you take that
33:33into account or as general knowledge.
33:36That should be listed a lot. Give me a
33:39moment, I want to do a procedure for a
33:41moment. Please, if you have any
33:48questions, you can write them or
33:49whoever is in charge can ask me the
33:51question if you wish. Is anyone alive
34:02there? It seems not. Let's continue. So
34:08, patneumonic morphological findings in
34:13the peripheral lamina. This is
34:16important. Although it is true, I have
34:20already found the hemoglobin, I have
34:22already found the BCN greater, but in
34:24the peripheral lamina I can find these
34:26hypersegmented neutrophils, that is,
34:28they have more than five lobes. This is
34:35a cell line of megaloblastic anemia or
34:37macrocytosis, that is, erythrocytes
34:39with increased volume. Yes, that is
34:46found in the peripheral lamina and that
34:48is a marker that is even said to be
34:50highly sensitive for detecting early
34:52macrocytic changes. This one even says
34:56that it is pathocytic. So, if I have a
35:01peripheral lamina with these findings,
35:03the hemoglobin is high, the BCM is
35:05increased and these two, I can already
35:07say that it is megaloblastic anemia.
35:11There I would need to define if it is
35:13due to a B12 deficiency or a
35:14polycythemia deficiency, correct? Even
35:17here the theory says that a pathocytic
35:19finding is the presence of neutrophils
35:21with five more nuclear lobes. I was
35:25telling you a while ago that
35:27anisocytosis, variability in size, and
35:29laocytosis, variability in shape, will
35:31be present in this in various entities.
35:36So it is not typical of iron deficiency
35:38anemia, but hypochromia and
35:39microcytosis are. It is important to
35:45emphasize that the diagnostic
35:46sensitivity of these two values is more
35:48sensitive to avoiding significant
35:50macrocytic changes than even the BCN,
35:52that is, the peripheral layer is more
35:54important. Blood fraction. Currently,
36:06in the hospital we already have the
36:08dosage of B12 and folate, therefore, a
36:10timely and adequate acquisition of both
36:12deficiencies can be made. Here I
36:18mentioned it as a kind of culture as
36:19part of the information, but doing the
36:21B2O dosage allows us to make an
36:23accurate diagnosis of the efficiency of
36:25both. Here, sorry, here it talks about
36:33masking. What is masking? Although it
36:38is true that megaloblastic anemia is
36:40caused by a deficiency of B12 and
36:42polycystic acid, if I think there is a
36:44deficiency of polycystic acid and
36:46initial polycystic acid, the hemoglobin
36:48will be corrected. But neuronal damage,
36:54that is, damage to the spinal cord, to
36:56the neuron or the depletion, will occur
36:58, it will continue to occur, because I
37:00am not correcting B12, right? I am
37:05correcting polycystic acid to 92 and
37:07remember that B12 has to do with
37:09neuronal damage, therefore this damage
37:11will continue to advance and sometimes
37:13I can become irreversible. So, whenever
37:21I have a low hemoglobin level and a BCM
37:23greater than 100 or greater than 90,
37:25then I must always differentiate
37:27between B12 and folic acid, since if I
37:29treat with folic acid, I can partially
37:31improve the anemia, but not the
37:33neuropathy; therefore, it will be a
37:35continuous and irreversible production.
37:42This is masking. That is why it is
37:44important to have the deficiency
37:46diagnosed, whether it is one or both.
37:57Either the underlying cause of
37:58deficiency of B12 or folic acid. B12
38:03deficiency is the most common,
38:05malabsorption, malabsorption. And
38:10currently we have gastrointestinal
38:12surgery or gastric bypass because it is
38:14fashionable. Gastric bypass is
38:18generating many or several populations,
38:20it is increasing the prevalence of
38:22tests with anemia with B12 deficiency,
38:24but just in case I tell you that it is
38:26not only B12, it is also iron
38:30deficiency. Remember that the stomach
38:35is a basic process for both components,
38:37iron and B12, to be absorbed. So, what
38:42gastric bypass does is reduce this
38:49absorption and the absorption of both
38:51iron and B2. So, this is going to be a,
38:56if we continue with gastric bypass
38:58surgery, gastric bypass is likely to
39:00increase the prevalence of anemia. So
39:04malabsorption, pernicious anemia is a
39:06particular entity, that is already a
39:08specialty management. It is an
39:11autoimmune disorder that destroys the
39:13gastric parietal cells. Therefore, in
39:16order for B12 to be absorbed, it needs
39:19a component called intrinsic factor.
39:24Intrinsic factor is produced in the
39:25parietal cells of the stomach, so if
39:27this is destroyed, there is no
39:29intrinsic factor, therefore, B12 cannot
39:31be absorbed in the terminal hydrium.
39:34That is why it is important, this is
39:36called percise anemia and the treatment
39:38for this type is sports. Gastric
39:41surgery, as I already told you,
39:43gastrotomy or gastric grip, the ideal
39:45infection affects the solution of boils
39:47. We had already described celiac
39:51disease as strict veganism. The good
39:57thing about strict veganism is that in
39:58our country it is not yet such a big
40:00trend, it is something that I am sure
40:02you would like to talk to me about.
40:07I am sure that strict veganism is still
40:09maintained, it is not so common in our
40:11country, therefore it is not yet highly
40:16prevalent, but I have seen patients who
40:18come for their B2 ampoules. As a
40:22general idea, my concept is that we are
40:24carnivores because alcohol always
40:26provides us with what we need. So being
40:31a carnivore means that you depend
40:34physiologically on B12. And where do
40:37you find B2? Unfortunately, it is in
40:41meat, eggs, and milk. So, who provides
40:45meat? Animals, whether we like it or
40:48not, we must eat meat to have vitamin
40:50B2 in our bodies. And the deficiency of
40:54this folic acid, as I already told you,
40:57is 20%, has to do with green products.
40:59Above all, it is due to insufficient
41:02dietary intake: a diet low in green
41:05leafy vegetables, low in legumes, low
41:07in fruits, and, more common in the
41:10elderly, and alcohol, correct?
41:12Increased needs. I also mentioned that
41:17a deficiency of folic acid generates a
41:19deficiency in neural tubercles, which
41:21is why during pregnancy it requires an
41:23increase for full development.
41:27Increased electrolyte levels, yes, poor
41:30absorption, as well as B12, also have a
41:32lot to do with it. Celiac disease,
41:35erythropoiesis or intestinal retraction
41:38affect the use of drugs. Which drugs
41:43are frequently used that inhibit the
41:45absorption of folic acid? Antipeptides,
41:49sympathomimetics, salicylic acid,
41:52methotrexate in isoforms or autoimmune
41:55diseases. That is why methotrexate is
41:59frequently associated with the
42:01consumption of folic acid. Therapeutic
42:06management. I think you already know
42:08the therapeutic management, oral doses
42:17of ferrous sulfate or intravenous iron
42:19sucrose, depending on the type of
42:21treatment. I will now explain how this
42:24treatment should be given. For ferrous
42:27sulfate, I told you a moment ago that
42:29the minimum treatment is 3 months, the
42:31minimum, and the appropriate one is up
42:34to 6 months. Therefore, normally,
42:36during the consultation, what I do is
42:38give treatment for three months and in
42:40the fourth month I ask for a control
42:42blood count. And if I see that it has
42:44improved, I discharge him, but if I see
42:46that it has not, I give him three
42:47additional doses. Remember, I can
42:50recover hemoglobin or improve his
42:52hemoglobin in two weeks. Increase it by
42:56one mg, but the complete treatment is 3
42:59months. That should be considered as a
43:03kind of structure in the treatment. The
43:09current biographies recommend
43:11alternating doses versus daily doses.
43:16They even recommend giving them every
43:18other day or every other day. Remember
43:22that regarding iron, intolerance or
43:26non-compliance is due to digestive
43:29discomfort, most frequently
43:30constipation, folic acid or nausea. So,
43:35this may result in inadequate adherence
43:38to iron treatment. The advantages of
43:42alternating doses, as I was saying,
43:45every 48 hours, greater
43:46gastrointestinal tolerability, and
43:49reduced side effects. I already told
43:51you which ones, better fractional
43:53absorption and better adherence. The
43:55best adherence, remember, because of
43:57the discomfort, facilitates compliance,
43:59but if the person can tolerate it daily
44:01, it is also a good regimen. Every 48
44:05hours, the alternating dose and the
44:07daily dose, remember that it is a 200
44:10mg tablet, preferably morning and night
44:12in the first three months so that there
44:14is a good response. I was telling you
44:17that hemoglobin will improve in two to
44:19three weeks. That is not our goal. Our
44:24goal is that the iron deficiency that
44:25occurs should cover that deficit and
44:27replenish the iron stores in the body.
44:31That is the most important thing. That
44:35is why if someone is given treatment
44:37with their hemoglobin or women are
44:39monitored and their mulubina may be 11
44:41or 12 and they stop treatment, rest
44:43assured that in two or three months
44:44they will come back with anemia. I was
44:55already telling you that you should
44:57increase it by one milligram in two to
44:59three months, right? Sorry, in two to
45:01two weeks, increase it by one milligram
45:03, but that is not the important thing.
45:06I repeat that hemoglobin can increase,
45:08but the most important thing is the
45:13replenishment of iron in the body. The
45:17duration of treatment: correction phase
45:20of 2 to 3 months; replenishment phase,
45:22that is, filling the iron stores, from
45:253 to 6 months, also depending on the
45:27patient. If it is a vulnerable
45:30population, I sometimes have to give it
45:32for 6 months. For example, if I give
45:36the iron supplement morning and night
45:38and I see that the patient is
45:40intolerant because it causes greater
45:42prolongation, I can give it once a day,
45:44then the treatment is also extended to
45:466 months or longer. Here, look at this
45:52red part that says premature
45:54discontinuation and I already told you
45:56that if they give you an improvement
45:58and then stop taking it again, you will
46:00have a relapse of anemia. Intravenous
46:04iron has conditions. One indication
46:06would be, uh, sorry, the patient does
46:08not have indications, one of them is
46:10failure to take the oral route, that is
46:12, the patient is intolerant or does not
46:14tolerate oral treatment at all.
46:17Malabsorption or severe anemia, less
46:19than six or less than seven
46:21intravenously. And this also requires
46:24great care. What happens is that
46:27intravenous iron improves hemoglobin in
46:29a short period of time. But I reiterate
46:32, what I need is for the iron deposits
46:37that are already stored as savings in
46:43the liver, in the muscles, in the
46:45macrophages. I have to repopulate that.
46:47So, I can achieve that in 3 months. I
46:50give him intravenous iron, maybe in a
46:53week I have a good response. After
46:56three or four weeks or up to six weeks
46:58I do another blood count and most
47:00likely he has anemia. Remember, iron
47:06deficiency anemia is loss, blood loss.
47:09Where do I lose blood? Uh, I already
47:11told you, women of childbearing age
47:13through menstruation and in men.
47:16Gastrointestinal loss is what I have to
47:18do to make an accurate diagnosis. If I
47:22do not correct the cause, there is also
47:24a high probability of treatment failure
47:26. In the case of folate, the treatment
47:32of choice is 1 mg. Folic acid comes in
47:370.5 mg, so two tablets a day, it can be
47:40morning and night or it can be two
47:42tablets at 11 in the morning. It is the
47:46standard dose for correcting the
47:48deficiency. Well, and here they put the
47:53clinical warning of masking as a record
47:55. Remember that I can only start folic
47:58acid if I have ruled out a B12
48:00deficiency. The B12 can be by Bioral,
48:06Bioral is not used, what it does use is
48:10the ampoule, a 1 mg ampoule. Here it
48:13says one ampoule for 4 weeks, one
48:16ampoule weekly for 4 weeks. The
48:18treatment, according to some clinical
48:20guidelines that I have reviewed, I do
48:22it in the following way. One
48:25intramuscular ampoule daily for 7 days
48:28and then after the seventh day I wait a
48:30week and start one intramuscular
48:32ampoule for 4 weeks. Correct?
48:36Pernicious anemia, which I already told
48:39you is a deficiency of intrinsic factor
48:41, that is a lifelong management and
48:43will depend on how long the decrease in
48:46B2 takes. The decrease in B12 in the
48:50body, I normally do not consume
48:52products rich in B12, can cause 3 to 5
48:55years of loss of appetite. Turn this on
48:59, I can check them every 3 months, 9
49:05months or even 12 months and depending
49:07on that I will start the treatment.
49:13Okay, the comparative treatment table,
49:15right? Iron deficiency anemia, I
49:17already told you, oral supplementation
49:19with your own iron. Here is the
49:22alternating dose every 48 hours or also
49:24the daily dose. Considerations and
49:27alternatives. The daily dose is
49:29effective but with worse tolerability.
49:31That is true, intravenous iron fails
49:34the oral route, plus absorption or
49:36severe anemia. And regarding the
49:40response criteria, hemoglobin will have
49:42a better response in two weeks and
49:44normalization, and rifampin will only
49:46be given in three to six months. I
49:49reiterate, I emphasize, in three to six
49:52months. If you only give treatments for
49:54one month, you will have failure. A
49:58deficiency of 1000 grams of coumaric
50:00acid per day, correct? It will correct
50:03the anemia and normalize the serum
50:05calcium level. This is also faster with
50:08efficient treatment. Normalization of
50:12B12 levels, as I told you, involves
50:15seven intramuscular ampoules daily and
50:17one ampoule per four weeks,
50:19individualized. Remember that modern
50:23management moves away from a
50:24one-size-fits-all approach and adapts
50:26to the individual needs of the patient.
50:29Each patient will have different needs
50:33for immunotherapy and monitoring. The
50:36answer can be found, that is,
50:43hemoglobin can have an increase
50:45response in two weeks, two or three
50:47weeks, but ensuring that this
50:52hemoglobulin does not relapse is three
50:55to six months. Education and follow-up
51:00are already part of what we, the
51:02healthcare professionals, are
51:03responsible for stating the importance
51:05of anemia management or the recovery of
51:10hemoglobin, which I was telling you a
51:13while ago is important for cellular
51:15respiration. Adherence is the main
51:20barrier to therapeutic failure and a
51:22recurring problem. Regarding adherence
51:25to ferrous sulfate due to intestinal
51:27gas discomfort, we already know that
51:29adherence will not be good depending on
51:31the patient and, above all, the
51:33duration of the treatment, replenishing
51:35the body's iron reserves, not just
51:37normalizing hemoglobin. I can normalize
51:40hemoglobin even in a month, but the
51:42most important thing is to repair the
51:44reserves. This, once achieved in at
51:49least 3 months, has left each patient
51:51with 6 months of loss, and in the case
51:53of megaloblastic anemia, the treatment
51:56is lifelong. Here, even in the
52:01biography, they use the teachback
52:03method. What does it mean? Asking the
52:07patient to repeat the information in
52:09their own words to verify understanding
52:11and reinforce key messages, like this
52:13morning. Let's say we are highlighting
52:17some important things that should be
52:19taken into account. Effective
52:22communication strategies for treatment.
52:26Clear communication, nutritional
52:28counseling, and I reiterate here that
52:30the consumption of seven products per
52:33week, such as red meat, cigarettes,
52:35pork, beef, mushrooms, eggs, and milk,
52:38guarantees 80%of your hemoglobin.
52:42Management of side effects. In the case
52:44of iron associated with hypothyroidism,
52:47we could give them tulara or another
52:52product, whether natural, that helps
52:54manage the growth, right? Regarding
52:58rhythmic warnings, as long as the
53:00masking is a deficiency of vedose and a
53:02deficiency of folic acid. Regarding
53:06iron deficiency anemia, this is
53:08important, the best absorption for iron
53:10deficiency anemia is emu iron. Where
53:13can I find emu iron? Lean red meat,
53:16chicken and fish, seafood and mollusks.
53:22What I mentioned a while ago in our
53:24common Peruvian diet, lung, blood
53:26sausage, and champagne are good, good,
53:29good products to improve iron
53:31deficiency, right? Iron, noem. Oh, also
53:38this thing about vitamin C, vitamin BC
53:40is true, ascorbic acid allows better
53:43absorption of iron, so if it is
53:44preferable, treatment with vitamin C
53:47can be given, but the important thing
53:49is that the person takes it, that the
53:51treatment is taken. Vitamin C helps
53:53absorption, but the important thing is
53:55that the person takes it. While it is
53:57true that legumes, pecorino, spinach,
53:59broccoli, and fortified cereals have
54:02iron, not iron, but this is their
54:04content. It is low and does not produce
54:08the desired effect in the body. Let's
54:11say it is rude to make a comparison. If
54:15I eat 100 g of red meat or 100 g of
54:17blood sausage, it would be equivalent
54:20to 10 kg of lentils or 10 kg of lentils
54:23daily so that there can be good
54:25absorption. So, the most convenient
54:28products are these. That is why I told
54:31you a while ago that there are seven
54:33products that I suggest you consume.
54:35That in small quantities guarantee good
54:38absorption and as part of the culture,
54:40the consumers of iron absorption are
54:43tea, coffee, calcium, and tutas.
54:47Therefore, these should be kept away
54:49from foods, especially foods with type
54:52M. And for megaloblastic anemia, foods
54:54rich in folates, I already told you,
54:57all green leafy vegetables, legumes,
54:59beans, oranges and citrus fruits have
55:02folate. Foods rich in B1, I emphasize
55:05again, red meats, chicken, fish, eggs
55:08and dairy products and fortified
55:10products in babies. The monitoring
55:16protocol in two weeks I can have a
55:18theoretical public response by
55:20increasing hemoglobin. In 1 mg, in 2
55:25weeks I can have, that's why it's not
55:28my...within the clinical importance of
55:30this morning, it is in the replacement
55:32of hemoglobin stores. In a month I can
55:37even have 12 or more than 12, but rest
55:40assured that if I don't give him the 3-
55:42month treatment, in two or three months
55:44he will come back with anemia again and
55:46probably more severe anemia. Regular
55:50follow-up once discharged, check in 6
55:52months or a year. And in the case of
55:57pernicious anemia, as I told you,
55:59depending on the patient, some can be
56:01treated every 3 months, every 6 months
56:04or even 12 months in some. B12 so that
56:08there may be a deficiency or decrease
56:10in the body for a period of 3 to 5
56:12years. Well, these are reminder tools.
56:16Now that we are in fashion,
56:18applications, SMS, filing systems,
56:20short-form programs on cell phones so
56:23that they can have control. And finally
56:27, we are going to talk about what a
56:28specialized referral is. In what
56:31situations should I refer to a
56:32specialist? Neurological warning signs.
56:36This is an emergency when there is a
56:38deficit of B2 of acute combined
56:40generation of the spinal cord. B2
56:43deficiency can cause acute combined
56:45generation of the spinal cord, correct?
56:49A process that damages the muscles and
56:51motors. Therefore, I can have classic
56:55stability of symptoms, weakness in the
56:58extremities, atarxia and alterations in
57:00sensitivity. What is weakness and
57:04extremity? Loss of muscle strength.
57:07Right? Can't stand up anymore, can't
57:09walk anymore. Twitching, loss of
57:11coordination, balance, those who seem
57:13drunk, loss of coordination, balance
57:16and alterations of insanity, loss of
57:18vibration and propulsion, that is, they
57:21don't feel, perhaps, the pain threshold
57:23in their body has decreased. It says,
57:28urgent referral. Any compatible
57:30neurological sign is an indication for
57:32urgent referral for evaluation. It
57:34could be a neurologist or a
57:36hematologist. Any specialist can treat
57:39this problem, right? Other neurological
57:42symptoms, paresthesias. What is
57:44paraesthesia? Tingling or numbness with
57:47cognitive impairment, memory and
57:49concentration problems. I already told
57:52you this also occurs in parathyroid
57:54anemia. And in megaloblastic anemia,
57:56memory and concentration problems.
58:00That's why in older adults, sometimes
58:03when they have anemia, they forget or
58:05lose their memory and concentration,
58:07and they have changes in personality,
58:09irritability, depression, or appetite.
58:15But this is in more severe cases,
58:17especially pancytopenia and failure to
58:19respond to therapy. I mentioned to you
58:24a while ago what pancytopenia is. Pan
58:27is the prefix for everything, that is,
58:29the three types of cells in the
58:31bloodstream decrease. Therefore, there
58:35will be a decrease in erythrocytes,
58:37leukocytes, and platelets. Right? This
58:43is called pancytopenia, and this can
58:45have other implications, such as bone
58:47marrow problems or bone marrow
58:48infiltration. Right? So, this can be
58:53more profound. What causes or what
58:56other causes can cause pancytopenia?
58:59Apart from B12, myelodysplastic
59:02dysplasia, tumor infiltration,
59:04metastasis of other cancers through the
59:06bone marrow. The first and third are
59:10hematological entities. These
59:13underlying causes will cause
59:14pancytopenia and I should think about
59:16it. If I find not only anemia, it is
59:21advisable to refer the patient to a
59:23specialist because there may be other
59:25more complex conditions than B12
59:27deficiency and failure to respond to
59:29treatment. Persistence of anemia
59:33despite adequate treatment. As I was
59:36saying, before starting treatment I
59:38should even look for the cause, because
59:40if I do not treat the cause, the anemia
59:42will persist even if we fill her with
59:44tons of iron. What is the most frequent
59:47cause? Retinal hemorrhage, right? Or
59:50poor absorption. And in the case of
59:52fertile women, heavy menstruation. As a
59:57kind of teaching in the office, what I
1:00:00say is that menstruation should last a
1:00:02maximum of 5 days. The first three days
1:00:07can be heavy menstruation and the last
1:00:09two days are already irregular. A
1:00:12menstruation longer than 7 days is no
1:00:15longer normal. I always consider that
1:00:19after that they should have a tape with
1:00:21gynecology to see if they have any
1:00:23disorder. Uh, referral criteria as soon
1:00:29as they see the clinical part.
1:00:32Neurological signs, ataxia, weakness,
1:00:35B12 deficiency, spinal cord damage,
1:00:38specialty, no, you can no longer treat
1:00:41it. Pancytopenia, specialty. Failure to
1:00:45respond to treatment, to
1:00:46gastroenterology or hematology
1:00:48specialty to do complementary studies.
1:00:51Severe anemia due to management, when
1:00:53severe anemia should be referred to the
1:00:55hospital. Why? Because then it even
1:00:57requires a transfusion of packed red
1:00:59blood cells. Suspected malabsorption,
1:01:02gastroenterology to see if there is
1:01:04malabsorption, some disease or an
1:01:06enteropathy. Anemia of an elderly
1:01:08person. I already told you that
1:01:10neurodiplastic syndrome is more
1:01:12frequent in this, therefore refer to a
1:01:14hematologist and the initial
1:01:15cytological findings. In the peripheral
1:01:18lamina, if there are ring glaucoma or
1:01:20pancytopenia with glaucoma, that is the
1:01:23form. Well, Conía assures me, as I
1:01:36told you, rings, cyroblasts, BLOS,
1:01:40anemia in elderly patients and, among
1:01:45others, gastrointestinal ones. So,
1:01:48common and comprehensive management of
1:01:50anemias at the primary care level
1:01:52requires a systematic and
1:01:54evidence-based approach integrating
1:01:56accurate diagnosis and individualized
1:01:58treatment. We have been emphasizing
1:02:02this throughout this presentation. The
1:02:03correct interpretation of biomarkers
1:02:06such as hemoglobin, BCM, ferritin,
1:02:09saturin, right? Recognizing warning
1:02:13signs and timely referral are essential
1:02:15to optimize results. Accurate diagnosis
1:02:20, biomarkers and cell morphology,
1:02:22whether in iron deficiency anemia or
1:02:24megaloblastic anemia, effective
1:02:26treatment, evidence-based regimens, I
1:02:29already told you what they are, and
1:02:31comprehensive follow-up, that is,
1:02:33education and monitoring, a follow-up
1:02:36in 6 months. That would be the
1:02:39treatment of both iron deficiency and
1:02:41megaloblastic anemia. I think that's
1:02:43where the presentation ends. Yes,
1:02:44that's where the presentation ends. If
1:02:46you have any questions, I would like
1:02:48you to ask them or this concludes the
1:02:50presentation. Thank you very much.
1:02:54Thank you very much, Doctor, for this
1:02:56excellent teletraining. If we have
1:02:59questions in the chat, we are going to
1:03:01invite all participants to ask their
1:03:02questions through the chat. Let's start
1:03:05, Doctor, with the first question we
1:03:07have in our chat. I can hear you. Tell
1:03:13me
1:03:13clearly. Doctor. Patients with a
1:03:16possible diagnosis of arthritis,
1:03:18rheumatoid arthritis and polyarthralgia
1:03:20tend to suffer from anemia. What should
1:03:23these patients 'diet be? If there is a
1:03:30presumptive diagnosis, refer them to
1:03:32rheumatology, but I already told you a
1:03:34moment ago that chronic inflammatory or
1:03:36immune diseases, such as this case of
1:03:38rheumatoid arthritis, will cause anemia
1:03:40in the long term. Yes, they cause
1:03:45anemia. It is a condition. A patient
1:03:48with rheumatoid arthritis, even with
1:03:50treatment with rheumatoid arthritis,
1:03:52will have a folic acid deficiency and
1:03:54also an iron deficiency. Therefore,
1:03:57these chronic autoimmune disease
1:03:59conditions, be it lupus, rheumatoid
1:04:05arthritis or any chronic disease you
1:04:07can think of, will indeed cause anemia.
1:04:11That is true.
1:04:13Thank you very much, doctor, for your
1:04:15response. Let's move on to the next
1:04:17question. Vitamin B12 and folate, in
1:04:19what cases can they be requested? Oh, I
1:04:26told you, let's see, in specific cases,
1:04:29I think I mentioned in the presentation
1:04:31, if you have a blood count, check the
1:04:33BCM, sorry, the mean volume. If it is
1:04:40greater than 90 in 5, ask for B12 or
1:04:42folic acid and so, let's say
1:04:44empirically, elderly patients, over 65
1:04:47years old with anemia is most likely.
1:04:50Why? Because unfortunately, older
1:04:56adults can be adventurous or have
1:04:57difficulty eating meat, or else meat is
1:04:59hard to digest, and therefore older
1:05:01adults sometimes tend not to consume
1:05:03meat-rich products, and they will be
1:05:05anemic in the long term, especially
1:05:07with B12. Folic acid, not so much,
1:05:14because eating, say, lettuce, pickles,
1:05:16avocado will help because that is the
1:05:18green product that we need. And that is
1:05:22the percentage, 20%. So those would be
1:05:25some conditions, let's say, that I
1:05:27should highlight.
1:05:29Thank you very much, doctor. Let's move
1:05:31on to the next question. In a patient
1:05:34with 7%anemia, treated with iron
1:05:36sucrose, what will be its
1:05:38administration? For how long? The
1:05:41appropriate time to administer iron
1:05:43sucrose more than the treatment. Let's
1:05:45see, I hear you, I hear you.
1:05:47Yes, correct. Is it true that you have
1:05:49to cover yourself with a black garment
1:05:51because of the light? Let's
1:05:53see, regarding intravenous iron levels
1:05:58below 7, right? But I think it works if
1:06:02you present it to me like this, Teo
1:06:04saccharate says. Yes, but I have to
1:06:07repeat what the cause is, right? What
1:06:12is the cause of this anemia of 7?
1:06:14What's more, I could say that anemia of
1:06:177, he should receive regular packages.
1:06:20Perhaps the bad thing about that is
1:06:21that in the areas, for example, in the
1:06:23Santa Rosa Hospital we don't have an
1:06:25exclusive area for transfusions, so we
1:06:27have to send him to the emergency room
1:06:29and sometimes the emergency room is
1:06:30full. So yes, the minimum would be one
1:06:34or two globular packages. Intravenous
1:06:37iron does work, but before that I would
1:06:39like to know the causes of this anemia,
1:06:41because if not, what is the point of
1:06:43giving him intravenous iron if it is
1:06:45anemia due to B12 deficiency? Now, if
1:06:50you have already diagnosed that it is
1:06:52anemia due to iron deficiency, the
1:06:54ideal is more or less 200 mg of iron
1:06:57saccharate, uh, diluted in 250 cm c of
1:06:59sodium chloride for 5 days; But it does
1:07:01have to be administered every 2 to 3
1:07:04hours because it can sometimes cause
1:07:06adverse effects in the patient. It's
1:07:11like a kind of management, right? But I
1:07:14think that management should be done by
1:07:16a specialist or in a hospital; it
1:07:17doesn't seem to me that it's for the
1:07:19periphery.
1:07:24Thank you very much, doctor. Let's move
1:07:27on to the next question. According to
1:07:30the latest research, will alternating
1:07:32doses of iron have a positive effect on
1:07:34the treatment of anemia in children
1:07:35under 2 years of age? No, let's see,
1:07:41the alternating dose that I'm giving
1:07:43you is a dose for adult or older adult
1:07:45patients. In children under 2 years of
1:07:49age, treatment should be daily and it's
1:07:51given in drops. So, let's see, but I
1:07:55repeat, you also have to look at anemia
1:07:58in a child because it's, right? The
1:08:03cause, always the cause, look for the
1:08:05cause, don't just give it out there in
1:08:07the populations, apart from women of
1:08:09childbearing age and adults or older
1:08:11adults, there is a peak in anemia in
1:08:12the pediatric population. The peak in
1:08:17anemia begins at 6 months due to
1:08:19breastfeeding. It seems to me that they
1:08:22have added liver to the diet. Before,
1:08:25it was, or I don't know if it is still
1:08:27mashed bananas or potatoes, when what
1:08:29they need is protein and protein, if
1:08:35they can give them liver, pâté would
1:08:37be adequate. So, the alternating dose
1:08:46due to the loss that ferrous sulfate
1:08:48can produce, yes, it can be, but
1:08:49remember that this alternating dose
1:08:51will have an extension in the treatment
1:08:53. The normal is 3 months, perhaps it
1:08:59will be prolonged for more months, also
1:09:01depending on the diet. It is a joint
1:09:08treatment, the iron will be taken out,
1:09:11sorry, the plate in drops plus the diet
1:09:13. Everything is a comprehensive
1:09:15management. I think that management
1:09:17should go to a specialist.
1:09:22Right, doctor, thank you very much for
1:09:24your answer. Let's move on to the next
1:09:25question. What should be done for a
1:09:29patient who has had anemia for 10 years
1:09:31and has not managed to reach the normal
1:09:32hemoglobin range, what treatment or
1:09:34what can be the most important thing?
1:09:37The most important thing I think I said
1:09:39in the presentation is that when there
1:09:41is failure, refer the patient to a
1:09:42specialist. I repeat that the treatment
1:09:45of anemia is the diagnosis of the cause
1:09:47; the cause of anemia is what I should
1:09:49do. If I have the cause, I treat the
1:09:53cause better than anemia. If I don't
1:09:57find the cause and no matter how much
1:09:59treatment I give her, whether I give
1:10:01her tons of iron or B12 or cholic acid,
1:10:03I won't find any improvement. For
1:10:09example, if I have a patient, a young
1:10:11woman of childbearing age, whose
1:10:13periods last more than 10 days, even if
1:10:15I give her plenty of iron, I will never
1:10:17see any clinical improvement because
1:10:19the loss, although not, uh, the loss of
1:10:21iron is greater due to bleeding than
1:10:23consumption; therefore, she will have
1:10:25chronic anemia no matter how much iron
1:10:27I give her. Now, if you tell me that it
1:10:34has been more than, I think you said
1:10:36more than years, I think I heard 7
1:10:38years or more, then that patient should
1:10:40at least see a specialist because other
1:10:41causes must be looked for. And if it's
1:10:45an older adult, I can think of plastic
1:10:47anemia, I can think of myelodysplastic
1:10:49syndrome. So, it's not from this type
1:10:54of position to tell you to give him
1:10:56treatment or what you should do in
1:10:58terms of therapeutic management. I
1:11:02don't dare say it. What I would suggest
1:11:05is that you seek out a hematologist
1:11:06specialist and see what the cause is.
1:11:12Right, doctor, thank you very much for
1:11:14your answer. Let's move on to the next
1:11:16question. They're asking us, what is
1:11:19your opinion on iron consumption in
1:11:21causing colorectal cancer? In fact,
1:11:28cancer, just as they asked me about
1:11:30rheumatoid arthritis, cancers cause
1:11:32anemia, right? Yes, they cause anemia.
1:11:37So, more than iron treatment, it's
1:11:39combined treatment. In cancer, I can
1:11:42have a deficit of all three products.
1:11:46So, just as you asked me about that
1:11:48patient who had been suffering from
1:11:50anemia for a long time, I would suggest
1:11:52monitoring his anemia profile and
1:11:54treating him accordingly, because it
1:11:56could not only be iron deficiency, but
1:11:58also B12 and folic acid deficiency. And
1:12:04yes, in cancer patients, they do have
1:12:06long-standing anemia and treatment must
1:12:08be given as much as possible to improve
1:12:10it. Now, if I add chemotherapy to that
1:12:17cancer, chemotherapy will also cause my
1:12:19levels to drop, it will cause
1:12:21pancytopenia, that is, low hemoglobin,
1:12:23low leukocytes, and low...The treatment
1:12:26is continuous, even for life, right?
1:12:30Because remember that depending on the
1:12:32type of cancer, the prognosis is not
1:12:34very good.
1:12:37Thank you very much for the
1:12:38clarification, doctor. Let's go to a
1:12:40consultation. They are presenting us
1:12:42with a case, a nutritionist is writing
1:12:44to us, he is asking us how he could
1:12:46explain the information that I am going
1:12:48to give him next, right? It is a
1:12:50warning, a 13-year-old patient has been
1:12:52observed, right? In an automated blood
1:12:56count, his red blood cell count was
1:12:59greater than 5.5 million, his
1:13:00hematocrit was 14.6, BCM 61 and MCH 26.
1:13:08I could not explain a
1:13:11removal of 14.6.
1:13:14Okay.
1:13:15Could you please explain to me if this
1:13:17information is associated with anemia?
1:13:19Let's
1:13:19see, first, BCM, how much were you
1:13:21telling me? Below 70 I think you said,
1:13:23right?
1:13:24Yes, BCM 61.
1:13:26Okay. Very good. And MCH
1:13:2926.
1:13:31Okay. It is very easy to explain.
1:13:37Remember that the values that you have
1:13:39mentioned in a blood count, first,
1:13:40there is a low population, I think they
1:13:42told me now, of 12-year-olds.
1:13:4813 years old, doctor.
1:13:4913 years old. Very good. That is, let's
1:13:53say, an indirect way of saying that it
1:13:55will be iron deficiency anemia in the
1:13:58long term if there is no control. What
1:14:02happens is that, in iron deficiency
1:14:09anemia, although it is true that the
1:14:11hemoglobin may be normal, the levels or
1:14:13reserves are decreasing. Therefore, I
1:14:19may have these values, as you can see,
1:14:21decreased, which tells me that in the
1:14:23long term I will be, that is to say, in
1:14:26the initial or primary stage of anemia
1:14:28and that it will cause anemia in the
1:14:30course of one to two months. It is an
1:14:34initial stage. Now, why could I have
1:14:37anemia in 13 years? Very simple, they
1:14:39are in the process of growth and
1:14:41development. They have a greater
1:14:43consumption for the formation of
1:14:45hemoglobin. Therefore, the reserves
1:14:47will be mobilized and will decrease.
1:14:52What these levels are telling you is
1:14:54that iron reserves will be decreasing
1:14:56and therefore if there is no timely
1:14:57management, it will cause consequent
1:14:59anemia. Remember that erythrocytes
1:15:04range from 4 million to 6 million. 5
1:15:08million is in the middle, but according
1:15:10to the values you told me, it is
1:15:12probably because the iron is decreasing
1:15:14and if you give him treatment in
1:15:16sequence for three to six months it
1:15:18could cause anemia.
1:15:24Thank you very much, doctor, for your
1:15:26response. Let's move on to the next
1:15:28question. They are asking us, "Doctor,
1:15:30good afternoon. Blood sausage is used
1:15:34to treat low hemoglobin, however, there
1:15:35are times when it is indicated that it
1:15:37can cause cancer. How true or false
1:15:40would that be? We know that blood
1:15:43sausage is the main food to treat
1:15:44anemia.
1:15:48It is a falsehood. We mostly have false
1:15:52myths in formation, depending on who
1:15:54has told you. If a doctor tells you, it
1:15:58is questionable, but if the neighbor
1:16:00next door or someone who is not a
1:16:02doctor tells you, why believe them?
1:16:04Blood sausage is very good. Cancer,
1:16:07although it is true, in some
1:16:09biographies it is mentioned that meat
1:16:11has a lot to do with cancer, it is not
1:16:13fully proven. Meat does not cause
1:16:18cancer, it would be, let's say,
1:16:24terrifying to say that meat causes
1:16:26cancer or blood sausage. That is
1:16:30misinformation that does not take into
1:16:32account within the medical field. As a
1:16:36hematologist I do not have a basis or,
1:16:39let's say, a magazine or evidence-based
1:16:41information that mentions that. It has
1:16:44nothing to do with it. to see. Neither
1:16:47red meats, blood sausage, liver, or
1:16:49blood vessels have anything to do with
1:16:51cancer at any level. What they do do is
1:16:56provide treatments when cancer has
1:16:58already been diagnosed, which is
1:16:59prohibited due to another component.
1:17:03That is why the management of the
1:17:06primidines produced by meats has
1:17:08another way of being managed when
1:17:10cancer is present, but it has not been
1:17:12proven that it causes cancer. There is
1:17:15no valid systematic review that can
1:17:17tell you that it is true that blood
1:17:19sausage causes cancer. That is total
1:17:22misinformation.
1:17:25Thank you very much, doctor. We are
1:17:27also going to discuss another case that
1:17:29a user is sharing with us. He tells us
1:17:32that he has a 19-year-old patient with
1:17:35vitamin B12 of 386.1, hemoglobin of
1:17:4011.9, BCM of 89.1, hematocrit of 37.
1:17:43What suggestions do you have for
1:17:46treatment? For treatment, not so much,
1:17:51first the diagnosis of 19 years with
1:17:53B12 deficiency, the cause must be
1:17:56sought. I insist again, please
1:17:57understand that it is not just about
1:17:59giving treatment, because I am being
1:18:01told that the patient is 19 years old.
1:18:03It is not necessary to give treatment,
1:18:05but to look for the cause. At 19 years
1:18:07old, I must look for the cause. For
1:18:12example, a while ago I mentioned that
1:18:14patients with BH have B12, patients I
1:18:17was talking about 328 or above, 300,
1:18:19B12 for what is in outpatient treatment
1:18:22. Yes, I start treatment. Uh, I usually
1:18:27consider an average of 400. B12, normal
1:18:30values range from 200 to 1100 or 900
1:18:33and something, a lab child, let's say,
1:18:361000, uh, 300, to me it seems like a
1:18:39deficit, therefore, I should give him
1:18:42treatment. But before treatment, the
1:18:44most important thing, I reiterate, I
1:18:47emphasize, I repeat, look for the cause
1:18:49. 19 years old, risky social behavior.
1:18:5319 years old may have a deficit, uh, uh
1:18:56, intrinsic factor, therefore,
1:18:58pernicious anemia. Uh, 19 years old,
1:19:02what else can I think? That he has some
1:19:05Problem of poor absorption or some
1:19:07intestinal problem, parasites? I should
1:19:10look for the causes, not just say," Oh,
1:19:12I'll start treatment and that will help
1:19:14it improve. "It's not that simple." Hey
1:19:17, if you could suggest what the first
1:19:19step is for that patient, refer them to
1:19:21a specialist to evaluate them because
1:19:23it should be a complete evaluation.
1:19:26They could be doing low-level testing,
1:19:28they could have an infectious problem,
1:19:35etc. Thank you very much, doctor, for
1:19:42your response. We want to thank all the
1:19:44participants.
1:19:45Good morning. Any other questions?
1:19:47No, doctor. We have now closed the
1:19:49round of questions. We want to thank
1:19:52you for answering each of the
1:19:53participants' questions.
1:19:56We want to thank Dr. Carrasco for this
1:19:58excellent teletraining. To conclude
1:20:02this session, doctor, we would like to
1:20:04ask you for some final recommendations
1:20:06for all the participants. Let's see, uh
1:20:11, although it is true that I am
1:20:12addressing the first level of care, uh,
1:20:15first I would like to congratulate them
1:20:17and first ask them how the filter is,
1:20:19uh, an hemogram, I think it is already
1:20:26nationwide. It seems to me that, as far
1:20:28as I understand, communication is
1:20:30massive. At this moment I do not know
1:20:34how many of you are reading and
1:20:35listening, but a blood count is
1:20:37important. Therefore, Diagnosing anemia
1:20:41is very important for vulnerable
1:20:43populations, children or pediatric
1:20:45patients, women of childbearing age and
1:20:48older adults. A hemoglobin level below
1:20:5211, depending on sex or, excuse me,
1:20:54whether male or female, is considered
1:20:57anemia. So, use the BCM if you do not
1:21:00have the complete profile, for example,
1:21:04iron, perrithin, transferrin, P12 and
1:21:06folic acid. And according to the BC BCM
1:21:09, you can establish whether it is iron
1:21:11deficiency or megaloblastic anemia and
1:21:13start treatment. The most common is
1:21:15iron deficiency anemia. Start treatment
1:21:20with your 300 mg dose, morning and
1:21:22night for 90 days and do a check-up and
1:21:25see if you want a hemoglama, a
1:21:30hemoglobin that has improved in two or
1:21:32three weeks, but the complete treatment
1:21:35lasts at least 3 months, right? And
1:21:38always check adherence. I think that
1:21:41would be the final message. How kind,
1:21:45doctor, for your response. We deeply
1:21:47appreciate Dr. Carlos Carrasco Veray
1:21:49for sharing his experience and
1:21:51knowledge on the comprehensive
1:21:53management of anemia. Your presentation
1:21:56was very clear, Doctor, and in any case
1:21:58, it will contribute to daily clinical
1:22:00practice. It has been a pleasure,
1:22:03Doctor. We hope to have you with us in
1:22:05the next session as well.
1:22:06Thank you very much. See you later.
1:22:12Good afternoon, Doctor. We would also
1:22:16like to thank all the participants and
1:22:18remember to subscribe to our YouTube
1:22:19channel Telesalud Mina
1:22:21Telecapacitaciones, and also visit our
1:22:23social networks to stay informed about
1:22:24upcoming educational activities. Thank
1:22:28you very much to everyone. Today's
1:22:30session is now concluded.

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This page contains the full transcript of ANEMIA by Telesalud Minsa Telecapacitaciones, generated from the public captions YouTube serves with the video. The transcript has 11,143 words across 1,760 segments, with the original timestamps preserved so you can click any line to jump to that moment in the embedded player.

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Use the transcript to take notes, quote the speaker, build a study guide, generate a summary with ChatGPT or Claude via the YouTube Summary tool, or export it as a timed subtitle file with YouTube to SRT. You can also re-open it in the transcriber to choose a caption track available on the video.

Free YouTube transcript tool

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