Shadowing Practice: Introduction to Hematology - Learn English Speaking with Video

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All right, hi everyone.

Now that we've finished the cardiovascular unit, we want to have a quick introduction to hematology.

We're going to go through some of the material from chapter 28.

There's quite a lot to be done for hematology,

and you'll have a whole unit later on in the year that covers the basic conditions related to hematology.

So this is really a lecture that's going to give you

some of the basics of blood cell formation for red blood cells, white blood cells, and also platelets.

We'll talk a little bit about the regulation of their production, their breakdown, and some of the common lab tests and clinical applications.

This is by no means going to give you everything you need to know for hematology, but should be a quick introduction to get you started.

So hematology is the study of blood, including the formation, function, and disease of the components of blood.

So the key structures we're talking about here are red blood cells, white blood cells, platelets, and the lymphoid organs and tissues.

remember that we have already had a lecture on blood vessels

and blood so if you haven't yet watched that lecture please go back

and watch it this will cover the basic components of blood

which are summarized here in textbook figure 28 .1 so remember

that whole blood includes plasma which is mostly water but also proteins

and solutes and then we have the formed elements of blood

which are mostly erythrocytes or red blood cells

but also very importantly the white blood cells

and platelets white blood cells are also referred to as leukocytes and

if you review the blood lecture you'll see the different forms of leukocytes where we describe how to tell them apart

So the leukocytes are neutrophils, lymphocytes, monocytes, eosinophils, and basophils.

We also talk about mast cells and related cells like natural killer cells.

Later this week, with Sam's lecture, you guys are going to talk about the immune system.

And Sam's going to quiz you guys on the blood.

So you want to study this and make sure you're ready before we start the immune system.

So we're now going to focus on blood cell production.

So hematopoiesis is the formation of new blood cells.

About 100 billion new cells per day.

These are produced in the fetal liver and the spleen, and after birth primarily in the red bone marrow.

You'll also hear the red bone marrow referred to as active marrow

and tissues that produce blood cells are referred to as myeloid tissues.

Red bone marrow is only in select bones the pelvis the vertebrae the cranium the mandible sternum ribs

and proximal ends of the humerus and the femur.

Hematopoietic stem cells like other stem cells undergo mitosis differentiation and maturation to become the final cell type.

Cells will then travel out of the bones to enter the general circulation and the lymphoid tissues.

So hematopoietic stem cells are the stem cells in the bone marrow that can produce all blood cell types.

They have self -renewal in the bone marrow.

Growth factors and cytokines stimulate differentiation of stem cells to progenitor cells

and the progenitor cells then give rise to specific precursors

which often have a portion of their name as blast

and then mature cells which often have a portion of their name as site

or fills so let's look here at this figure from your textbook

so we start with the hematopoietic stem cells

and then based on a number of factors will begin to differentiate into progenitor cells.

Those progenitor cells will then undergo a number of other changes

to slowly progress into each of the possible cell types formed by the bone marrow.

So here you can see several of the leukocytes, the platelets, here's the red blood cells, and other types of leukocytes.

We're going to get into some of these details now.

One note here is that I don't expect you guys in any way to memorize the factors that lead to this differentiation.

This might come up later in some treatments that you will use, but it's much more advanced level than what you guys need for now.

So let's first talk about red blood cell production.

So erythropoiesis is formation of red blood cells in the bone marrow.

Whereas hematopoiesis is formation of all cells, erythropoiesis is specific to red blood cells.

About 2 .5 million red blood cells are produced every second.

And this is stimulated by the hormone erythropoietin.

Do you remember when we talked about EPO?

So remember EPO is secreted by the kidneys and the liver when oxygen levels are low.

The last step in red blood cell production, if we follow our progenitor cells,

is going from reticulocytes to erythrocytes.

So that's the final step.

Notice the internal changes in the cell before the cell becomes an erythrocyte.

So both internal changes to the nucleus and the organelles until the cell is finally an erythrocyte,

which has very few organelles and is packed with hemoglobin.

It also has its final size and shape.

Reticulocytes will circulate for a short period of time before they become red blood cells.

This takes about 24 to 48 hours

so normally about 1 % of circulating red blood cells are reticulocytes that's a normal number

that you'd see in your labs if this number increases

that gives an indication

that there's more red blood cell production going on than normal like a lot of other growth

and cellular changes erythropoiesis has vitamin and nutrition requirements.

Let's look at some of the vitamins.

Erythropoiesis requires vitamin B12.

This is required through dietary intake.

It's transported by intrinsic factor protein, which we talked about briefly when we talked about the stomach, and it's stored in the liver.

B12 can be stored for quite a long time before it's required for dietary intake.

folate on the other hand is quickly depleted it's a component of nucleotides needed for DNA

and RNA synthesis and because cell production including red blood cell production requires DNA

and RNA synthesis folate is required as well so b12

and folate deficiencies can lead to anemias and I'll show you that in a moment.

Other vitamins that are required are listed here.

Vitamin B6, riboflavin, pantothenic acid, niacin, ascorbic acid, vitamin E.

In addition to the vitamin requirements, there's also hemoglobin synthesis that happens requiring protein and iron.

Hemoglobin synthesis increases within differentiating erythrocytes up to the reticulite state, reticulocyte stage.

So remember that hemoglobin is made up of heme and globin chains.

So heme requires ferrous iron and the types of hemoglobin are based on these chains.

So hemoglobin A is the most common form in adults.

It's 92 percent of adult hemoglobin and it's made up of alpha 2 and beta 2 chains.

There are other forms of hemoglobin that you will learn as you progress through this clinical program.

In particular, you will learn from our hematologists that hemoglobin changes through embryonic field development and into childhood and adulthood.

So keep this in mind as you look at some of the conditions later on in hematology.

because hemoglobin requires iron there's also it's also important for us to review the iron cycle

so 67 percent of total body iron is bound to hemoglobin so

if a 25 milligram daily requirement for erythropoiesis we get about

one to two milligrams from our diet absorption through the intestines is regulated by a hormone called hepcidin.

The rest is obtained through iron recycling.

So how this works is that free iron in the plasma binds to transferrin.

apotransferrin and iron becomes transferrin.

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Transferrin then carries the iron to the bone marrow and releases it for hemoglobin production.

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Iron is also stored as ferritin in macrophages.

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Apopherritin plus iron forms ferritin.

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Aggregates of ferritin micelles are hemocydrin deposits and we would see these histologically

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when a tissue is bruised when it's iron rich or

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if there's accumulation in certain pathological conditions red blood cells live about a hundred to a hundred

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and twenty days which means there needs to be a quite active process for red blood cell breakdown

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so red blood cells are broken down by the spleen

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or the cup for cells in the liver they're taken up by macrophages

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and they're broken down to heme iron

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and globin the iron will be oxidized the globin will be broken down into amino acids

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and the heme will be broken down into bilirubin

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if you go back and review our digestive lecture you'll see

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that we also describe bilirubin excretion in the digestive lecture bilirubin

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is ultimately excreted through bile from the liver to the intestines into the feces.

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Some can be reabsorbed in the intestines as urobilinogen and will be excreted from the kidneys via urine.

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Reduction in red blood cells or in their oxygen carrying capacity through disruption of hemoglobin causes anemias.

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So anemias can be caused by low red blood cell production.

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This could be iron deficiency, chronic inflammation, B12 deficiency, folate deficiency,

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stem cell dysfunction, infiltrates to the bone marrow, many reasons why you might have low red blood cell or hemoglobin production.

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Anemias can also be caused by acute or chronic blood loss.

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And finally, anemias can be caused by increased red blood cell breakdown or hemolysis.

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Remember lysis means breakdown.

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Later, not now, but later, you will learn how to read the peripheral smears to look for changes in blood cell phenotype.

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Are they too small?

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Are they too big?

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Are they too light in color?

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And this will help you to determine what type of anemia your patient may have.

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You guys will get good at this during the hematology unit.

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So when you come back for the hematology unit, you can refer to these figures from your textbook.

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The key terms here will be how big is the cell?

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So erythrocyte volume, is it a normal size?

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Normocytic.

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Is it too big?

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Macrocytic.

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Or is it too small?

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Microcytic.

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So we would say these are normocytic anemias, macrocytic, or microcytic anemias.

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And you can classify your conditions based on that.

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We also look at the hemoglobin content.

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Normal, would be normochromic, too much would be hyperchromic, and low would be hypochromic anemias.

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There's many lab tests for red blood cells and for hemoglobin.

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It's actually quite easy once you get used to it, but getting the tests down can be complicated.

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So a lot of this has to do with how many cells are there and what do the cells look like.

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So there's straight cell counts, red blood cell counts, there's the size of the cells in mean corpuscular volume, and the amount of hemoglobin.

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Further on down we can do more tests on the hemoglobin.

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We can look for precursor cells like reticulocytes,

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which can help us understand bone marrow function and some other tests as well.

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There are also lab tests for hemoglobin.

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So there are tests which look at iron for iron deficiency anemias.

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We can look at ferritin and transferrin.

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We can look at anti -antiglobulin tests and antibody screens.

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There's many different ways to also test for hemoglobin and

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And what I like about your textbook is that it tells you what the test is for and the possible cause.

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So as you're learning about all of your different anemias, you can put this together into the lab tests and the test results that you're seeing.

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I should say, I'm not requiring you guys to know this right now.

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I'm giving it to you so that you have it in your back pocket for later.

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I will not test you on the lab tests for red blood cells and hemoglobin, or the other tests I give in this lecture for that matter.

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But I want you to know

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that we can test for many different portions of what's going on with the cells

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and how the cells and the cell numbers are changing.

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Alright, on to white blood cells.

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White blood cells are leukocytes.

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Leuco means white.

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They arise from two main groups of progenitor cells.

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So if we look here, back at this figure for the hematopoietic stem cells,

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you can see that we have myeloid progenitor cells and lymphoid progenitor cells.

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So the lymphoid progenitor cells ultimately give rise to the lymphocytes,

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the B cells and the T cells which are going to be very important to understand for your immune system lecture.

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They also give rise to the natural killer cells and the plasma cells which are again important in the immune system.

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The myeloid progenitor cells are going to give rise to all of the other white blood cells the neutrophils,

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the macrophages monocytes, eosinophils, and basophils.

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These are also important for immune function, but not for the adaptive immunity that we'll be discussing next week.

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So the production of white blood cells increases in response to infections,

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steroid hormones, reduction of cells in the marrow as a reserve pool.

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As you learn the functions of the white blood cells, it will help you to understand why they increase and decrease with various lab tests.

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So we look at a differential white cell count, the absolute number of each type of leukocytes within the blood,

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and we can see the numbers of neutrophils,

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lymphocytes, monocytes, eosinophils, basophils, and also plasma cells as a function of various conditions.

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All right, on to platelets.

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So we're going to talk about production and breakdown as well for platelets

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so platelets again are produced in the bone marrow from hematopoietic stem cells

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and pointing here so you can find them in the pathway

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so they come from myeloid progenitor cells

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which give rise to these huge cells called megakaryocytes one megakaryocyte breaks off about a thousand platelets from its cytoplasm

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Platelet production is increased by the hormone thrombopoietin, TPO, which is released by the liver and stimulates the bone marrow.

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Platelets are broken down by macrophages in the spleen and the liver and they have a lifespan of about 10 days.

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Overall about two -thirds of the total platelets are in circulation and about a third are in the spleen.

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But you can see sequestration of platelets under various conditions and your hematologist will talk you through that.

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The most important function of platelets is hemostasis.

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And I want to spend a lot of time here on hemostasis

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because understanding clot formation is very key to understanding a lot conditions

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so hemostasis is a cascade of steps that stops bleeding

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so hemo means blood stasis means stop

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so the blood vessels are a closed system

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and any damage to a blood vessel will be quickly plugged by the hemostasis cascade

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so that blood volume blood pressure and blood flow can be maintained

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so damage to a blood vessel triggers hemostasis you've already heard quite a lot about clot formation from our pathologist,

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but let's talk about the specific steps involved.

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There are six steps here which are summarized in this figure of your textbook.

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We're going to go through each of those steps in the next few slides.

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So first there's an injury to the vessel.

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So there's some kind of exposure of the

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subendothelial layer this is the layer just under the endothelium this

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causes the smooth muscle in the blood vessel wall to contract

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platelets can then begin to fill the gaps this contraction

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or vascular spasm will reduce the blood flow to the area

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and will be most effective in small vessels not so much in the large vessels.

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It's stimulated by thromboxin A2 and it's inhibited by prostacycline and nitric oxide.

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The second step is platelet adhesion.

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Von Willebrand factor and other adhesive proteins bind the platelets to collagen in the vessel wall.

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This is stimulated by a number of factors including throboxyn A2, epinephrine, thrombin, and collagen.

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Essentially these platelets are becoming sticky and they're sticking to the collagen wall.

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So in this image here you can see the endothelium.

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There's been damage to the endothelium such that the sub -endothelial layer is exposed

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and here's that basement layer and then the smooth muscle below

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and the platelets are now sticking to that collagen within the connective tissue deeper in the blood vessel layers.

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Step three is activation of the platelets.

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Platelets are not simply fragments of cells.

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They are actually quite active.

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They will change shape.

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They will swell.

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They'll become spiky.

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They'll increase adhesion and aggregate to the fibrinogen and von Willebrand factor.

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This is again stimulated by thromboxin A2 and ADP.

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So here are the platelets activating and changing shape.

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Step four is continued adhesion and aggregation of the platelets.

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So this is like a positive feedback system.

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As platelets are recruited, more and more platelets come in.

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The activation then of the coagulation factors begins.

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Thrombin and fibrin will become active.

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Fibrin mesh will then form.

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So remember that fibrin forms this mesh over the clot.

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Finally, as the fibrin becomes more dense, stronger, it forms the platelet plug.

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So here, when we have this stronger fibrin mesh,

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the platelets adhered, and also you may get some blood cells and other nearby cells adhering,

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then we have a full platelet plug closing off that injured vessel wall, and that forms the full clot.

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This happens within three to five minutes of the initial blood vessel injury occurring.

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The last step is clot retraction and clot dissolution.

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So we don't want these clots to stay around.

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So the actin and myosin filaments will contract within the platelets packing and increasing the strength of the clot.

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The vessel walls will then be joined together by contraction

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and plasmin will be activated to begin dissolving that fibrin to degrade the clot.

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The activation of plasmin is done by a factor called TPA and the degradation of fibrin releases cleavage products including D -dimer.

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Some of you may have heard of TPA as a molecule

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that is used to dissolve clots in some conditions

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and as D -dimer as a test which can be used if a clot is suspected.

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So the purpose here is to get the blood vessel walls back together and then remove the clot.

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The blood clotting pathways are complex.

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There are two pathways that ultimately lead to formation of this fibrin mesh forming the blood clot.

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There's an intrinsic pathway which is stimulated by endothelial damage, for example arteriosclerosis.

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This starts with clotting factor 7 and goes to 10.

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Excuse me, clotting factor 12 and goes to 10.

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And then the extrinsic pathway is stimulated by external injury to the blood vessel, for example some kind of cut or laceration.

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This starts with clotting factor 7 and goes to 10.

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The final common pathway is factor 10 and factor 10 leads to the conversion of thrombin from prothrombin.

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Thrombin then converts fibrinogen into the fibrin mesh.

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So ultimately this is what leads to the formation of the fibrin mesh.

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All of these clotting factors listed here in the clotting cascade.

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All I want you to know right now are the intrinsic versus extrinsic pathway in general,

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what factors are involved, and that the common pathway is factor 10.

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Then finally the prothrombin to thrombin which leads to fibrinogen to fibrin.

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So I'm not going to ask you about each one of the factors now

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but these may come up later for you clinically

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so it's something to keep in mind the most important part is the formation of the fibrin mesh

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which ultimately forms that platelet plug and the clot

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so the reason we want you to take a look at the clotting cascade now is

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because of clotting and hypercoagulability in patients so increased clotting and hypercoagulability leads to a risk for thrombus formation.

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Thrombocytosis is a condition where you have excessive platelets.

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This can happen post splenectomy, when there's activation of the bone marrow, in certain cancer conditions, and during inflammation.

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There's also increased coagulation.

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That ultimately means sluggish blood flow.

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This can happen for many, many reasons.

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Immobility, sedentary lifestyle, post -operative patients, high estrogen states, and heart failure.

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If you have venous coagulation, often in the lower extremities, this can cause a venous thrombus or clot formation in the vein.

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If it's in a deep vein, it's DVT or deep vein thrombosis, which we have already talked about many times as a risk for pulmonary embolism

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because the way that those thrombus can give off emboli which can go through the right heart to the lungs.

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Clots in the arteries for example associated with atrial fibrillation can be risk for cerebral embolism or stroke.

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There are also bleeding and decreased clotting conditions.

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So this can happen because of decreased platelet numbers or thrombocytopenias.

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For example, decreased synthesis, sequestration of platelets by the spleen, increased breakdown, blood transfusions, HIV infections,

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certain drugs can all lead to thrombocytopenias.

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Thrombocytopenias, or defects in platelet number, ultimately can cause hemorrhagic problems, excessive bleeding and bruising.

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This can also happen because of platelet dysfunction.

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So platelet dysfunction can be caused by antiplatelet therapies, aspirin, NSAIDs, or high nitrogenous waste levels, for example, during renal failure.

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Finally, just as increased coagulation can be problematic, decreased coagulation can be problematic.

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So deficiency in various clotting factors,

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inherited hemophilias, or deficiency in von Willebrand factor can lead to decreased coagulation.

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Many factors are also also synthesized by the liver.

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So cirrhosis or liver disease can cause decreased coagulation.

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Finally vitamin K deficiency, vitamin K is required for certain coagulation factor function, can also decrease coagulation.

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Much of this can begin to be sleuthed out by looking at the different lab tests for platelets and clotting factors.

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So there are certain tests that look at the platelet count and also the timing for the coagulation cascade to progress.

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So there are many studies which look at the ability of platelets to aggregate

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and also the amount of time it takes for various the coagulation cascade to happen.

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Again, I'm not going to test you right now on the lab test for platelets and clotting factors.

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I just want you to know that these tests are available And as you learn about these different disorders,

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you can then link those disorders to some of these lab test results.

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Okay.

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Again, as I said, just a quick introduction.

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We have a lot more to do for hematology, but for now, this is where we are, and this is enough.

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Let me know if you have any questions.

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המלץ על סרטון

103 משפטים

אוצר מילים והערות הגייה לשיעור הזה

שיעור הדיבור הזה ברמה C1 מבוסס על הסרטון “Introduction to Hematology”. המילים שחוזרות הכי הרבה: cell, blood, platelet, factor, test. בסרטון הזה יש 301 משפטים ו-3739 מילים לתרגול Shadowing. הדיבור נמשך 29:46. הדובר שומר על קצב יציב של כ-126 מילים בדקה, קצב נוח לתרגול Shadowing. רק 77% מהמילים נמצאות בין 3,000 המילים הנפוצות ביותר באנגלית, כך שאוצר המילים מאתגר.

אוצר מילים מרכזי בסרטון הזה

15 המילים המתקדמות ביותר בסרטון, עם ההגייה והמשמעות שלהן:

מילה	הגייה	משמעות
platelet שם עצם	/ˈpleɪt.lət/	טסית
vitamin שם עצם	/ˈvɪt.ə.mɪn/	וִיטָמִין
leukocyte שם עצם	/ˈluːkə(ʊ)sʌɪt/	תא דם לבן, לויקוציט
erythropoiesis שם עצם		אריתרופויזה
spleen שם עצם	/spliːn/	טחול
textbook שם עצם	/ˈtɛkst.bʊk/	סֵפֶר לִמוּד
hormone שם עצם	/ˈhoɹmoʊn/	הורמון
plasma שם עצם	/ˈplæzmə/	פְּלַזְמָה
differentiation שם עצם	/dɪf.əˌɹɛn.ʃiˈeɪ.ʃən/	הבדלה
intestine שם עצם	/ɪnˈtɛs.tɪn/	מְעִי
bleed פועל	/ˈbliːd/	דִּימֵּם
vein שם עצם	/veɪn/	וְרִיד
contraction שם עצם	/kənˈtɹækʃ(ə)n/	התכווצות
organelle שם עצם	/ˌɔɹ.ɡənˈɛl/	אברון
summarize פועל	/ˈsʌməˌɹaɪz/	סיכם

דקדוק בסרטון הזה

המבנים שהדובר משתמש בהם הכי הרבה, עם המילים המדויקות מהסרטון:

מבנה	בסרטון
משפטי תנאי (Conditional sentences) if + clause, will/would + verb — תנאי ותוצאה שלו	if you review the blood lecture you'll see
סביל (Passive voice) be + past participle — הדגש הוא על מה שקורה, לא על מי שעושה את הפעולה	be done · are summarized · are also referred
משפטי זיקה (Relative clauses) who / which + clause — מידע נוסף על אדם או דבר	plasma which is · days which means · cells which are
הווה מושלם (Present perfect) have/has + past participle — פעולה שקרתה בעבר ועדיין יש לה חשיבות או השפעה עכשיו	we've finished · have already had · you've already heard

הגייה ששווה לשים לב אליה

הדובר משתמש ב-31 קיצורים וצורות מקוצרות, כמו we're, I'm, you'll. אמרו אותם בצורה הקצרה, כפי שאתם שומעים אותם.

הצלילים של “th”: pathway /ˈpæθˌweɪ/, erythrocyte /əˈɹɪθɹəˌsaɪt/, thrombin /ˈθɹɒmbɪn/, synthesis /ˈsɪnθəsɪs/, thrombus /ˈθrɑmbəs/
הצלילים של “sh” ו-“zh”: coagulation /koʊ.æɡjuˈleɪʃən/, deficiency /dɪˈfɪʃənsi/, mesh /mɛʃ/, activation /ˌæktəˈveɪʃən/, adhesion /ˌædˈhiː.ʒən/
מילים ארוכות — שימו לב להטעמה: hemoglobin /ˌhimoʊˈɡloʊbɪn/, coagulation /koʊ.æɡjuˈleɪʃən/, progenitor /pɹoʊˈd͡ʒɛn.ɪ.tɚ/, anemia /əˈnimi.ə/, hematology /ˌhiməˈtɒləd͡ʒi/

צלילים שדוברי עברית מתקשים בהם:

/w/ — שפתיים מעוגלות, לא /v/: pathway /ˈpæθˌweɪ/, quiz /kwɪz/
/æ/ — פתוח יותר מה-“אֶ” העברית, לא כמו “a” ב-“cup”: marrow /ˈmæɹəʊ/, coagulation /koʊ.æɡjuˈleɪʃən/, pathway /ˈpæθˌweɪ/, cascade /kæsˈkeɪd/, macrophage /ˈmækɹɔʊː.feɪd͡ʒ/
/r/ — הלשון לא נוגעת בשום מקום, לא ה-“ר” הגרונית: marrow /ˈmæɹəʊ/, fibrin /ˈfaɪbɹɪn/, progenitor /pɹoʊˈd͡ʒɛn.ɪ.tɚ/, erythrocyte /əˈɹɪθɹəˌsaɪt/, thrombin /ˈθɹɒmbɪn/

איך לתרגל עם הסרטון הזה

הקשיבו לכל הסרטון פעם אחת בלי לדבר, ורשמו את המילים שאתם לא מכירים.
תרגלו Shadowing משפט אחר משפט במהירות רגילה, וחזרו על כל משפט עד שהקצב שלכם תואם את הדובר.
הקליטו את עצמכם והשוו למקור, תוך תשומת לב למילים כמו platelet, vitamin, leukocyte.

מהי טכניקת השאדואינג?

שאדואינג היא טכניקת למידת שפה מבוססת מדע שפותחה במקור להכשרת מתורגמנים מקצועיים ופופולרית על ידי הפוליגלוט ד"ר אלכסנדר ארגואלס. השיטה פשוטה אך עוצמתית: אתה מקשיב לאודיו באנגלית ילידית וחוזר עליו בקול רם מיד — כמו צל העוקב אחרי הדובר עם עיכוב של 1–2 שניות בלבד. בניגוד להאזנה פסיבית או תרגילי דקדוק, שאדואינג מכריח את המוח והשרירים בפה לעבד ולשחזר דפוסי דיבור אמיתיים בו זמנית. מחקרים מראים שזה משפר משמעותית את דיוק ההגייה, האינטונציה, הקצב, הדיבור המחובר, הבנת השמיעה ושטף הדיבור — מה שהופך אותו לאחת השיטות היעילות ביותר להכנה לIELTS Speaking ולתקשורת באנגלית בעולם האמיתי.

טכניקת Shadowing: קרא את המדריך המלא שלב אחר שלב →

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