Microcytic And Normocytic Anemia Quiz

TIBC stands for Total Iron Binding Capacity. This term refers to the maximum amount of iron that can be bound to transferrin, a protein responsible for transporting iron in the blood. By measuring TIBC, healthcare professionals can assess the body's ability to transport and bind iron, which is crucial for diagnosing conditions such as iron deficiency anemia. The other options, total iodine binding capacity, total calcium binding capacity, and total vitamin binding capacity, do not accurately represent the meaning of TIBC.

TIBC stands for total iron binding capacity. This term refers to the maximum amount of iron that can be bound to transferrin, a protein that transports iron in the blood. TIBC is a laboratory test that measures the level of transferrin in the blood, providing information about the body's ability to transport and bind iron. It is often used to assess iron deficiency or iron overload conditions.

Other clinical presentations of Fe deficiency anemia include fatigue, pallor and SOBOE (short of breath on exercise). More serious presentations include glossitis, cheilosis and spoon nails.

with beta Thalassemia minor, there is decreased synthesis of the beta-globulin chain. In beta Thalassemia major, there is a total absence of synthesis for the beta-globulin chain.

Electrophoresis is a laboratory test that can be used to confirm the diagnosis of Thalassemia. Thalassemia is a genetic blood disorder that affects the production of hemoglobin, leading to abnormal red blood cells. Electrophoresis is a technique that separates molecules based on their size and charge, allowing for the identification of abnormal hemoglobin variants present in Thalassemia. This test can help differentiate between different types of Thalassemia and provide valuable information for the diagnosis and management of the condition.

serum ferritin increases in infection, inflammation, malignancy, liver disease, hyper TSH & hemochromatosis/Fe overload. Serum iron varies daily. TIBC is highly specific for decrease Fe, measures total amount of transferrin in blood. Saturation is serum Fe divided by TIBC - would be low in Fe deficiency.

G6PD hemolytic anemia is caused by oxidative stress. G6PD (glucose-6-phosphate dehydrogenase) is an enzyme that helps protect red blood cells from damage caused by reactive oxygen species. When there is an imbalance between the production of reactive oxygen species and the ability of G6PD to neutralize them, oxidative stress occurs. This oxidative stress can lead to the destruction of red blood cells, resulting in hemolytic anemia. Infections and reductive stress are not directly associated with the development of G6PD hemolytic anemia.

Fetus blood uses HbA and HbF - as HbF converts to adult type in infancy, the beta thalassemia defect is revealed.

Pancytopenia is a condition characterized by a decrease in all three types of blood cells (red blood cells, white blood cells, and platelets). It is not specifically associated with microcytic anemia, which is a condition characterized by smaller than normal red blood cells. Microcytic anemia is commonly caused by thalassemia, iron deficiency anemia, and anemia of chronic disease. Lead poisoning can also lead to microcytic anemia. Therefore, pancytopenia is the correct answer as it is not directly related to microcytic anemia.

The correct answer is duodenum. The duodenum is the first part of the small intestine where most of the iron absorption takes place. It is responsible for breaking down food and absorbing nutrients, including iron, into the bloodstream. Iron is an essential mineral for various bodily functions, such as oxygen transport and energy production. Therefore, the duodenum plays a crucial role in ensuring adequate iron absorption for the body's needs.

Infection is not an etiology of Fe deficiency anemia. Fe deficiency anemia occurs when there is a lack of iron in the body, which is needed for the production of red blood cells. The main causes of Fe deficiency anemia are chronic blood loss, increased requirement (such as during pregnancy or rapid growth), malabsorption (when the body is unable to absorb iron from the diet), and decreased intake (not consuming enough iron-rich foods). Infection does not directly cause Fe deficiency anemia, although it can contribute to anemia indirectly by causing chronic inflammation or affecting the body's ability to absorb or utilize iron.

When someone is missing all 4 genes for alpha-Thalassemia, it leads to a condition called hydrops fetalis. Hydrops fetalis is a severe form of anemia that occurs in fetuses and newborns. It is characterized by abnormal fluid buildup in the body, causing swelling and potentially leading to heart failure. This condition is often fatal, resulting in stillbirth or death shortly after birth. Additionally, the absence of these genes prevents the production of the alpha-Hb protein, which is essential for normal red blood cell function.

A bone marrow biopsy is the most reliable method to diagnose aplastic anemia. This procedure involves extracting a small sample of bone marrow from the hipbone or sternum and examining it under a microscope. It helps determine the number and quality of blood cells being produced in the bone marrow. Aplastic anemia is characterized by a decrease in all types of blood cells, and a bone marrow biopsy can confirm this by showing a reduction in cellularity and abnormal cell development. Other tests like blood smear and CBC can provide additional information, but a bone marrow biopsy is essential for an accurate diagnosis.

The lab reports indicate low mean corpuscular volume (MCV), high serum ferritin, and low total iron-binding capacity (TIBC). These findings are consistent with anemia secondary to inflammation. Inflammation can lead to increased ferritin levels as a result of iron trapping within cells and decreased TIBC due to reduced iron availability for binding to transferrin. This type of anemia is commonly seen in chronic diseases such as infections, autoimmune disorders, and malignancies. Fe deficiency, thalassemia, and hemoglobinopathy are less likely causes based on the given information.

The correct answer is "ability to absorb increases". In iron deficiency anemia, the body tries to compensate for the lack of iron by increasing its ability to absorb iron from the diet. This is done through upregulation of iron transporters in the intestines, allowing for enhanced absorption of iron. As a result, the total iron-binding capacity (TIBC) increases as the body tries to capture and transport more iron for utilization. This increase in TIBC is a response to the iron deficiency and is a compensatory mechanism to maintain iron homeostasis in the body.

Most non-heme iron in the body is found bound to transferrin. Transferrin is a protein that helps transport iron in the blood. It binds to iron and carries it to various tissues and cells in the body, where it is needed for various functions. This binding of iron to transferrin helps to regulate iron levels and prevent iron toxicity.

The correct answer is "haemolysis". Normocytic anemia can also be caused by the destruction of red blood cells, a condition known as haemolysis. This occurs when red blood cells are destroyed at a faster rate than they can be produced, leading to a decrease in overall red blood cell count and resulting in anemia. Other causes of normocytic anemia include acute blood loss, bone marrow failure, and chronic disease.

beta thalassemia minor (heterozygote) is usually asymptomatic.

Heinz bodies are abnormal structures that form within red blood cells. They are composed of excess alpha chains of hemoglobin. Normally, hemoglobin consists of two alpha chains and two beta chains. However, in certain conditions such as thalassemia or unstable hemoglobinopathies, there can be an imbalance in the production of alpha and beta chains. The excess alpha chains can precipitate and form Heinz bodies, leading to red blood cell damage and potential hemolysis.

HbH: 4 BETA chains
Hb Barts: 4 GAMMA chains

Citric acid and ascorbic acid enhance Fe absorption. Citric acid is a weak organic acid that forms soluble complexes with iron, making it easier for the body to absorb. Ascorbic acid, also known as vitamin C, can reduce iron from its ferric form to the more easily absorbed ferrous form. Both citric acid and ascorbic acid can increase the bioavailability of iron in the diet, helping to prevent iron deficiency.

ALL OF THEM! muahaha. Can also look at bone marrow stained with Prussian blue, which would show decreased macrophage iron and decreased or normal sideroblasts.

On the physical exam, you would not find splenomegaly or lymphadenopathy - unlike leukemia.

Beta thalassemia is a genetic disorder that affects the production of hemoglobin, leading to abnormal red blood cells. Heinz bodies are denatured hemoglobin that forms within the red blood cells, and their presence indicates oxidative damage. Target cells are red blood cells with a bullseye-like appearance, which can be seen in beta thalassemia due to abnormal cell membrane structure. Hypochromic microcytic cells are red blood cells that are pale and smaller than normal, which is a characteristic finding in beta thalassemia. Therefore, the presence of Heinz bodies, target cells, and hypochromic microcytic cells on a blood smear would be expected in beta thalassemia.

yes, all. Also: paroxysmal nocturnal haemoblocinuria (PNH). Chemotherapy drugs have a dose-response severity. The inherited disorder is called Fanconi's anemia.

Beta thalassemia is a genetic blood disorder that affects the production of hemoglobin, resulting in anemia. It is most commonly found in regions where malaria is or was prevalent, as the genetic mutation that causes beta thalassemia provides some protection against the disease. The Mediterranean region, Arabian peninsula, and southeast Asia are all areas where malaria has historically been present, hence the high prevalence of beta thalassemia in these regions.

The correct answer includes three treatment options for aplastic anemia: IV equine ATG, bone marrow transplant, and immune suppression. IV equine ATG refers to intravenous administration of antithymocyte globulin, which helps to suppress the immune system and prevent it from attacking the bone marrow. A bone marrow transplant involves replacing the damaged bone marrow with healthy cells from a donor. Immune suppression involves using medications to suppress the immune system and prevent it from attacking the bone marrow. These treatment options aim to improve the production of blood cells in individuals with aplastic anemia.

To confirm, you can do electrophoresis for HbH and/or Hb Barts.