 Welcome to MetSmarter lecture series. Today we will talk about high-yield hematology measures that are heavily tested on the exams. Before we start just take a minute and subscribe so you can get notified when we post a new video. So let's dig in. Our first image over here is of acentocyte cells. Acentocytes are irregularly shaped non-circular cells. They can arise from either alterations in the membrane lipids or structural proteins. Alterations in the membrane lipid are seen in abere lipoproteinemia and liver dysfunction. Liver dysfunction, apolipoprotein A2 deficient lipoprotein accumulates in plasma causing increased cholesterol in RBCs. This causes abnormalities of the membranes of RBC causing remodeling and in the spleen and formation of the acentocytes. In abere lipoproteinemia there is deficiency of lipids and vitamin E that is going to cause the abnormal morphology of RBCs. Then we have ikinocyte. Ikinocytes are your same looks like acentocytes. But the difference over here is they exhibit central pallop or lightning of the color in the center. They may be found in apolipidemia caused by liver dysfunction but lipids themselves do not integrate in the membrane. Instead it is speculated that cell surface receptors on the RBCs bind with HDL cholesterol which induces the shape change. We are going to see birth cells in uremia and chronic kidney disease, liver disease such as cirrhosis, partway kinase deficiency and in hyperlipidemia. Next we have tear drop cells. Tear drop cell formation is that RBCs containing various inclusions undergo pitting by the spleen to remove these inclusions and in the process they can be stretched too far to return to the original shape. It is also thought that this can similarly occur when RBCs with large inclusions are obstructed from passing through the micro circulation and the portion containing the inclusion gets pinched leaving a tail end. So you can see that over here, tailed end. As tear drop cells they are associated with myelofibrosis and myelodysplastic syndrome. So as they are associated with myelofibrosis they are also theorized to be formed due to mechanically squeezing out from the bone marrow as a result of the infiltrative process. Next we have schistocytes also known as helmin cells. They occur as a result of mechanical destruction of a normal RBC. This occurs when there is damage to the blood vessel and a clot begins to form. The formation of fibrin strands in the vessels occurs as part of the clot formation process. RBC cells get trapped in the fibrin strands and the sheer force of the blood flow causes the RBCs to break. And the resulting fragmented cells is known as schistocytes. So we can see an irregularly shaped jagged and have two pointed ends. So this is our helmin cells. Where do we find these? We find these in disseminated endravascular coagulation, thrombotic thrombocytopenic perpura, microinjapethic hemolytic anemia, hemolytic uremic syndrome, and malfunctioning cardiac rolls. Next we have elliptocyte. So elliptocyte are abnormally shaped RBCs. They appear oval or elongated. They form slightly egg-shaped to rod or pencil forms. They have normal centri-power with the hemoglobin appearing concentrated at the ends of the elongated cells. The ends of the cells are blunt and not sharp like sickle cells. Where do we find them? In heredity, elliptocytosis, talosemias, and ardent deficiency. The next we have spherocytes. Spherocytes is a sphere shaped rather than biconcave disc shape as normal. Spherocytes are found in immunologically mediated hemolytic anemias like in heredity spherocytosis. So what we see over here that the mishap, the L-healthy RBCs are mistaking by this plane for old or damaged RBCs. Anesthes constantly breaks them down causing the cycle whereby the body destroys its own blood supply. A complete bulk count will show increased reticulocytes. It's a sign of RBC production, increased RBC production if you're going to see increased reticulocyte count, decreased hemoglobin and hematocrit. We are talking about our heredity spherocytosis where we have direct positive Coombs test. Next we are talking about target cells. They are also known as chlorocytes. Our RBCs that have the appearance of a shooting target with the bull's eye. Target cells may appear in association with liver disease, alpha and beta talocemia, hemoglobin C disease, iron deficiency anemia, post-isplanectomy, auto-isplanectomy. Liver disease, we have activity of enzyme that is known as lecithin cholesterol acyl transphase that is going to be decreased in obstructive liver disease. Decrease enzymatic activity increases the cholesterol to phospholipid ratio and producing an increased surface area of the RBC membrane or maybe increased red cell fluidity. And in post-isplanectomy, a major function of our spleen is the clearance of opsonized, deformed and damaged throcytes by splinic macrophages. If a splinic macrophage function is abnormal or absent because of isplanectomy, altered spherocytes will not be removed from the circulation. So therefore we are going to see increased numbers of target cells. In auto-isplanectomy, that is going to be caused by sickle cell anemia or hypospalanism and celiac disease. Same reason will be there. Major function of a spleen is the clearance of opsonized or damaged throcytes. But now if they have auto-isplanectomy, where do we see like sickle cell anemia? So we will see a lot of numbers of target cells. Next we have sickle cell. Sickle cell is our rigid sickle shape. Okay? And it's the most common type is known as sickle cell anemia. It is going to be as a result of an abnormality in oxygen-carrying protein that is hemoglobin. This leads to a rigid sickle cell shape. Probs of the sickle cell disease typically begins around five to six months of age. A number of health problems may develop. Maybe that's known as sickle cell crisis like anemia, swelling of the hands and feet, bacteria and factions and stroke. So these are some characteristics of our sickle cell anemia. Next we have hovel jolly body. So hovel jolly body is a cytopathological finding of basophilic nuclear remanence. It's known as cluster of DNA in circulating RBCs. During maturation in the bone marrow, later through blasts normally expel their nuclei. But in some cases a small portion of DNA remains. Its presence usually signifies a damaged or absent spleen because a healthy spleen would normally filter this type of RBCs because the function of a spleen is to filter out damaged RBCs. This DNA appears as basophilic, the purple spot on an otherwise isnophilic pink erthrocyte. These inclusions are normally removed by spleen. Okay? But it will present in individual functional hyposplenemia or resplenia. So where are we going to see? We are going to see how it will jolly bodies in sickle cell anemia patients and patients who don't have a spleen or hyposplenemia. Next peppenheimer bodies. These are abnormal basophilic granules of iron that is found inside the RBCs on routine blood stain. There are type of inclusion body composed of ferritin aggregates or mitochondria or phagosomes containing aggregated ferritin. They appear as dense, blue, purple granules within the RBCs and they are usually one or two. Look at that one or two located in the cell periphery. We are going to see these bodies in cydroblastic anemia. Do not confuse that with hovel jolly body. In hovel jolly body you can see a single rounded spot. Over here we can see that we have one, two, three dots. Next we are talking about bite cells. Bite cells is an abnormally shaped mature RBCs with one or more semicircular portions removed from the cell margin and that's how they are known as bite cells and they are going to be as a result from processes of oxidative hemolysis such as in a condition of glucose 6-phosphate dehydrogenase deficiency. In this condition there is uncontrolled oxidative stress that's going to cause the hemoglobin to denature and form hinds bodies. These bites result from the mechanical removal of denatured hemoglobin during splinic filtration as red cells attempt to migrate through endothelial cells from splinic cords into the splinic sinuses. So the function of spline was to remove the damage or non-functional RBCs. So when they have those hinds bodies, spline is going to take the bite, splinic macrophages. Next hinds bodies. So what were the hinds bodies? These are inclusions within the RBCs composed of denatured hemoglobin like we were discussing in our previous slide. The presence of hind bodies represent damage hemolycobin usually through oxidative damage by administered or damaged by administered drugs and also we can see in glucose 6-phosphate dehydrogenase deficiencies. Thank you everyone. I hope this video was a source of information for you. Thank you.