Luyện nói tiếng Anh bằng Shadowing qua video: Introduction to Hematology

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.

100

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

101

Iron is also stored as ferritin in macrophages.

102

Apopherritin plus iron forms ferritin.

103

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

104

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

105

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

106

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

107

so red blood cells are broken down by the spleen

108

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

109

and they're broken down to heme iron

110

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

111

and the heme will be broken down into bilirubin

112

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

113

that we also describe bilirubin excretion in the digestive lecture bilirubin

114

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

115

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

116

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

117

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

118

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

119

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

120

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

121

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

122

Remember lysis means breakdown.

123

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

124

Are they too small?

125

Are they too big?

126

Are they too light in color?

127

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

128

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

129

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

130

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

131

So erythrocyte volume, is it a normal size?

132

Normocytic.

133

Is it too big?

134

Macrocytic.

135

Or is it too small?

136

Microcytic.

137

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

138

And you can classify your conditions based on that.

139

We also look at the hemoglobin content.

140

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

141

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

142

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

143

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

144

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.

145

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

146

We can look for precursor cells like reticulocytes,

147

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

148

There are also lab tests for hemoglobin.

149

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

150

We can look at ferritin and transferrin.

151

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

152

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

153

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

154

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.

155

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

156

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

157

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.

158

But I want you to know

159

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

160

and how the cells and the cell numbers are changing.

161

Alright, on to white blood cells.

162

White blood cells are leukocytes.

163

Leuco means white.

164

They arise from two main groups of progenitor cells.

165

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

166

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

167

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

168

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

169

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

170

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

171

the macrophages monocytes, eosinophils, and basophils.

172

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

173

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

174

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

175

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.

176

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

177

and we can see the numbers of neutrophils,

178

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

179

All right, on to platelets.

180

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

181

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

182

and pointing here so you can find them in the pathway

183

so they come from myeloid progenitor cells

184

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

185

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

186

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

187

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

188

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

189

The most important function of platelets is hemostasis.

190

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

191

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

192

so hemostasis is a cascade of steps that stops bleeding

193

so hemo means blood stasis means stop

194

so the blood vessels are a closed system

195

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

196

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

197

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

198

but let's talk about the specific steps involved.

199

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

200

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

201

So first there's an injury to the vessel.

202

So there's some kind of exposure of the

203

subendothelial layer this is the layer just under the endothelium this

204

causes the smooth muscle in the blood vessel wall to contract

205

platelets can then begin to fill the gaps this contraction

206

or vascular spasm will reduce the blood flow to the area

207

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

208

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

209

The second step is platelet adhesion.

210

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

211

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

212

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

213

So in this image here you can see the endothelium.

214

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

215

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

216

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

217

Step three is activation of the platelets.

218

Platelets are not simply fragments of cells.

219

They are actually quite active.

220

They will change shape.

221

They will swell.

222

They'll become spiky.

223

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

224

This is again stimulated by thromboxin A2 and ADP.

225

So here are the platelets activating and changing shape.

226

Step four is continued adhesion and aggregation of the platelets.

227

So this is like a positive feedback system.

228

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

229

The activation then of the coagulation factors begins.

230

Thrombin and fibrin will become active.

231

Fibrin mesh will then form.

232

So remember that fibrin forms this mesh over the clot.

233

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

234

So here, when we have this stronger fibrin mesh,

235

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

236

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

237

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

238

The last step is clot retraction and clot dissolution.

239

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

240

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

241

The vessel walls will then be joined together by contraction

242

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

243

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

244

Some of you may have heard of TPA as a molecule

245

that is used to dissolve clots in some conditions

246

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

247

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

248

The blood clotting pathways are complex.

249

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

250

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

251

This starts with clotting factor 7 and goes to 10.

252

Excuse me, clotting factor 12 and goes to 10.

253

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

254

This starts with clotting factor 7 and goes to 10.

255

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

256

Thrombin then converts fibrinogen into the fibrin mesh.

257

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

258

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

259

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

260

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

261

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

262

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

263

but these may come up later for you clinically

264

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

265

which ultimately forms that platelet plug and the clot

266

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

267

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

268

Thrombocytosis is a condition where you have excessive platelets.

269

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

270

There's also increased coagulation.

271

That ultimately means sluggish blood flow.

272

This can happen for many, many reasons.

273

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

274

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

275

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

276

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

277

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

278

There are also bleeding and decreased clotting conditions.

279

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

280

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

281

certain drugs can all lead to thrombocytopenias.

282

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

283

This can also happen because of platelet dysfunction.

284

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

285

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

286

So deficiency in various clotting factors,

287

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

288

Many factors are also also synthesized by the liver.

289

So cirrhosis or liver disease can cause decreased coagulation.

290

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

291

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

292

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

293

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

294

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

295

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

296

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

297

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

298

Okay.

299

Again, as I said, just a quick introduction.

300

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

301

Let me know if you have any questions.

✨ Video gợi ý

103 câu

Những Ấn Tượng Đầu Tiên

Video này là một tài liệu rất tốt cho việc rèn luyện kỹ năng nói tiếng Anh. Nội dung của nó không chỉ cung cấp thông tin về huyết học mà còn giúp bạn luyện nghe và phát âm tiếng Anh chuẩn. Cách trình bày rõ ràng, dễ hiểu và có tổ chức sẽ giúp người học dễ dàng nắm bắt kiến thức. Video mang tính giáo dục cao và tạo cơ hội cho người học tiếp cận với từ vựng chuyên môn, từ đó cải thiện khả năng giao tiếp trong các lĩnh vực liên quan.

Phân Tích Câu Chuyện

Hãy cùng phân tích một vài câu trong video để hiểu rõ hơn về cách chúng có thể giúp bạn luyện tập. Ví dụ, câu “Hematopoiesis is the formation of new blood cells.” (Tạo máu là quá trình hình thành các tế bào máu mới) giúp bạn nhận biết cấu trúc câu đơn giản nhưng vẫn chứa đựng ý nghĩa quan trọng. Cấu trúc này dễ nhớ và có thể được áp dụng trong nhiều ngữ cảnh khác nhau.

Câu khác như “These are produced in the fetal liver and the spleen.” (Chúng được sản xuất ở gan thai nhi và lá lách) là một ví dụ về cách diễn đạt thông tin cụ thể, giúp người học không chỉ phát âm mà còn hiểu được ngữ cảnh. Việc sử dụng các thuật ngữ chính xác như “fetal liver” hay “spleen” làm phong phú thêm vốn từ vựng của bạn, đồng thời giúp cải thiện kỹ năng shadowing tiếng anh.

Thói Quen Luyện Tập

Để cải thiện kỹ năng nói và phát âm, bạn có thể thực hiện một quy trình đơn giản nhưng hiệu quả. Hãy lặp lại và ghi âm những câu trong video. Bạn có thể làm theo các bước sau:

Bước 1: Nghe một đoạn ngắn từ video.
Bước 2: Dừng video và lặp lại câu đó, cố gắng sao chép ngữ điệu và nhịp điệu của người nói.
Bước 3: Ghi âm phần lặp lại của bạn.
Bước 4: So sánh âm thanh của bạn với âm thanh gốc để nhận diện sự khác biệt.

Quy trình này không chỉ giúp bạn nâng cao khả năng luyện nghe nói qua video mà còn cải thiện đáng kể kỹ năng phát âm tiếng anh chuẩn. Bạn có thể sử dụng phần mềm shadowing để hỗ trợ và theo dõi quá trình học của mình. Bằng cách này, bạn sẽ trở nên tự tin hơn trong việc giao tiếp bằng tiếng Anh.

Ngữ pháp trong video

Những cấu trúc người nói dùng nhiều nhất, kèm đúng cụm từ trong video:

Cấu trúc	Trong video
Câu điều kiện if + mệnh đề, will/would + động từ — điều kiện và kết quả	if you review the blood lecture you'll see
Câu bị động be + quá khứ phân từ — nhấn vào việc xảy ra, không phải người làm	be done · are summarized · are also referred
Mệnh đề quan hệ who / which + mệnh đề — thêm thông tin về người hoặc vật	plasma which is · days which means · cells which are
Thì hiện tại hoàn thành have/has + quá khứ phân từ — việc đã xảy ra nhưng còn liên quan đến hiện tại	we've finished · you've already heard · have already talked

Phương Pháp Shadowing Là Gì?

Shadowing là kỹ thuật học ngôn ngữ có cơ sở khoa học, ban đầu được phát triển cho chương trình đào tạo phiên dịch viên chuyên nghiệp và được phổ biến rộng rãi bởi nhà đa ngôn ngữ học Dr. Alexander Arguelles. Nguyên lý cốt lõi đơn giản nhưng cực kỳ hiệu quả: bạn nghe tiếng Anh của người bản xứ và lặp lại to ngay lập tức — như một "cái bóng" (shadow) đuổi theo người nói với độ trễ chỉ 1–2 giây. Khác với luyện ngữ pháp hay học từ vựng bị động, Shadowing buộc não bộ và cơ miệng phải đồng thời xử lý và tái tạo ngôn ngữ thực tế. Các nghiên cứu khoa học xác nhận phương pháp này cải thiện đáng kể phát âm, ngữ điệu, nhịp điệu, nối âm, kỹ năng nghe và độ lưu loát khi nói — đặc biệt hiệu quả cho người luyện IELTS Speaking và muốn giao tiếp tiếng Anh tự nhiên như người bản ngữ.

Phương pháp shadowing: đọc hướng dẫn từng bước đầy đủ →

Luyện nói tiếng Anh bằng Shadowing qua video: Introduction to Hematology

Physiology Chapter 1 | Introduction to Physiology & Homeostasis Explained

BLOOD TYPES explained in 9 Minutes

1. Introduction to statistics - Lecture 1

4 Subject Link 6 C1

Cerebral Vascular Anatomy And Imaging

Multiple Myeloma - signs and symptoms, pathophysiology, treatment

The Periodic Table: Crash Course Chemistry #4

Review of Musculoskeletal System (Bones & Muscles) - Biology Lectures Series

Human Anatomy Eye

SUMMARIZE SPOKEN TEXT - DNA & RNA

White Blood Cells (WBCs) - Your body’s Defense - Hematology

Endocrine System

Những Ấn Tượng Đầu Tiên

Phân Tích Câu Chuyện

Thói Quen Luyện Tập

Ngữ pháp trong video

Phương Pháp Shadowing Là Gì?