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EXAM #3 ANEMIA ONLY
MLT 126: HEMATOLOGY AND COAGULATION - ANEMIA/HEMOGLOBINOPATHY
| Question | Answer |
|---|---|
| Anemia can be defined as | lowered oxygen carrying capacity either due to improper erythropoiesis or hemoglobin production issues |
| Why would edema be present in some anemia clinical symptoms? | The body is attempting to compensate for low oxygen by increasing fluid volume |
| In acute blood loss anemia, why is anemia not immediately produced? | Extravascular fluids are being brought to peripheral circulation, allowing the body to adjust its TBV (causes Hct decrease) |
| Why would the RBC morphology for initial acute blood loss be normocytic/normochromic? | There isn't a bone marrow defect; the person is just losing a lot of blood |
| True or false: Within 48-72hrs, extravascular fluids moving into peripheral circulation cause decreases in Hct, Hgb, and RBCs with an increase in WBCs | true |
| Why would increased erythropoiesis occur over the next 3-5 days? | To compensate for the low oxygen tension; this will cause macrocytosis |
| What are some clinical findings found in chronic blood loss that differentiate it from acute blood loss | - iron deficiency anemia once the iron stores are depleted - normal or decreased WBCs, PLTS - normal or increase in retics |
| What would a CD 34 failure cause? | reduced growth and production of all blood cell lines (RBCs, WBCs, megakaryocytes |
| Define Aplastic Anemia | a bone marrow disorder that causes a decreased production of pluripotential or erythroid committed stem cells |
| What is the most common form of Aplastic Anemia? | Idiopathic |
| What kind of Aplastic Anemia can occur to those participating in Chemotherapy? | Iatrogenic |
| What are some infections that can cause Aplastic Anemia? | Hep B/C, measles, EBV, HIV, cytomegalovirus |
| What pathophysiological actions occur in Aplastic Anemia? | T-cells actively suppress proliferation of stem cells; this is tissue mediated specific organ destruction |
| What occurs in the phases of Aplastic Anemia | Onset: asymptomatic; surviving stem cells proliferate Recovery: stem cell volume does not increase, despite possible rebound Late disease: increased pancytopenia/myelodysplasia |
| What is the main clinical feature that would constitute total bone marrow failure? What risk do spontaneous acquire aplastic anemia patients undergo? | pancytopenia; increase susceptibility of acquiring malignant disease or future blood disorders |
| Pancytopenia, or the deficient production of all blood cell types, is the hallmark lab finding of WHAT anemia? How is it diagnosed? | Aplastic Anemia; if at least 2/3 peripheral blood values fall below critical values |
| What affect does Aplastic anemia have on the fibrotic bone marrow? | Very few megakaryocytes, myeloid, and erythroid cells can be seen |
| Depending on the stage of discovery, (blank) can be used to treat Aplastic anemia | transplant rejection drugs/immunosuppressant therapy |
| Aplastic anemia presents its RBCs as (blank). Why? | Normocytic, normochromic; the bone marrow is not producing enough RBCs |
| If there are a less than 1% of reticulocytes and less than 20 x 10^9/L platelets, what can you interpret from these findings? | likely pancytopenia; low retic=improper bone marrow response to anemia, low platelet count=megakaryocytes cannot mature correctly |
| HLA typing is used to determine DNA abnormalities for (blank) the most common aplastic anemia in children | Fanconi's Anemia |
| What are some prevalent clinical symptoms for children with Fanconi's anemia? | Stunted cognitive ability, skeletal malformation (particularly in their thumbs - a/hypoplasia), skin hyperpigmentation, low weight upon birth, short stature |
| What is the most notable lab finding in Fanconi's Anemia | pancytopenia that progressively shows itself by age 5, and Hgb leves of 5-6g/dL |
| True or false: Fanconi's Anemia, on a peripheral blood smear, will often have macrocytosis occurring | true |
| Describe Familial Aplastic Anemia | a subset of Fanconi's anemia that , although it does not cause any major developmental abnormalities, the bone marrow is hypocellular, resulting in pancytopenia |
| When we have a patient with PRCA (pure red cell aplasia), why would they have an increased serum EPO level? | Immunosuppression in Pure Red Cell Aplasia prevents the EPO from binding to precursor erythroid cells, inhibiting further erythropoiesis |
| Children under 8 years old are most affected by (blank), a temporary pure red cell aplasia caused by (blank) | acute (transient) erythroblastopenia of childhood; recurring viral infections |
| What are the lab findings integral to an Acute TEC diagnosis? | eythroblastopenia, reticulocytopenia, normocytic RBCs |
| In Diamond-Blackfan Syndrome, what is the root cause of it? | a gene mutation (RPS19) that causes congenital bone marrow failure |
| Describe some of the lab findings of Diamond-Blackfan Syndrome | - slow/progressive hypoplastic anemia (decreased production of RBCs), RBCs are normochromic and slightly macrocytic, normal WBCs and platelets |
| A hallmark lab finding of peculiarly shaped multinuclear erythroblasts would indicate towards what congential anemic disorder? What does it cause? | Congenital Dserythropoietic Anemia; indirect hyperbilirubinemia |
| What are the three major causes of anemia? | increased hemolysis, impaired RBC production, or blood loss |
| When does Iron Deficiency Anemia occur, and what can cause it? | When iron stores are depleted; this can be due to improper nutrition (in general, but especially when pregnant), excessive blood loss, or the iron cannot be absorbed properly |
| What is the range of total iron within an average adult? | 3.5-5g |
| What form of dietary iron has no heme, and its absorption is dependent on iron stores and dietary factors | iron salts |
| True or false: 10% of iron we get from food comes in the form of iron salts/ferric iron (Fe3+) | false; 90%=iron salts, 10%=heme iron |
| What is the difference between dietary and operational iron? | Operational=oxygen binding and biochemical reactions Dietary=extracted from food |
| Describe (broadly) how iron gets absorbed. | After its conversion from ferric (Fe3+) to ferrous (Fe2+), the iron passes through the stomach into the large intestine where it gets absorbed. From there, it forms a complex with transferrin and continues to move throughout the small intestines. |
| What are some clinical symptoms of IDA | papilledema (increase brain blood flow), pic (compulsive ingestion of nonnutritive substances) |
| True or false: In a peripheral blood smear, a patient with IDA can have normocytic normochromic RBCs | True; Normal RBCs can also become microcytic and hypochromic once the iron stores are fully depleted |
| True or false: Transferrin saturation and Total iron binding capacity (TIBC) has a inverse relationship in IDA lab findings | True; TIBC is increased because the transferrin is not saturated with iron, making the transferrin saturation decrease significantly |
| Why would Serum iron be significantly decreased in a patient with IDA? | there is more transferrin available for less iron |
| What is the second most prevalent anemia that is not associated with dietary deficiency? What can cause it? | Anemia of Inflammation or Chronic Disorders (ACD); malignancies, systemic disorders, infection, inflammation |
| True or false: ACD is a hypoproliferative anemia caused by underproduction of RBCs | true |
| What are some causes of ACD | - decreased erythropoiesis (either by cytokines suppression or halt of negative feedback loop) - decreased hepcidin production (causes functional iron deficiency) - decrease in rapid iron release from iron pools |
| In comparison to IDA, ACD has increase in ferritin. Why would that be? | The ferritin stores are not releasing iron as rapidly |
| Why would transferrin saturation be low in ACD like it is in IDA? | Iron is not released properly due to hepcidin deficiency, which produces dysfunctional iron |
| Which kind of anemia is a result of a mitochondrial defect that does not properly incorporate iron into Hgb, causing iron to encrust the nucleus of RBCs in bone marrow and also form Pappenheimer bodies? | Sideroblastic Anemia |
| How can we differentiate IDA from Sideroblastic Anemia in a PBS (peripheral blood smear) when they both have a low MCV/MCH value? | SBA: presence of normal platelets, codocytes, basophilic stippling (product of impaired production), dimorphic populations |
| What enzyme in hemoglobin synthesis will cause Sideroblastic Anemia (SBA), if its synthesis activity decreased? | Delta-ALA |
| What kind of microcytic, hypochromic anemia(s) would have elevated ferritin levels? Why? | ACD: because the ferritin stores are not being released as quickly SBA: iron is being precipitated and encrusting the nucleus of RBCs |
| What iron overload disorder is caused by a genetic metabolic error that causes excessive iron absorption? | Hereditary Hemochromatosis |
| In general, what are Megaloblastic Anemias a result of? | Imbalance in the nuclear/cytoplasmic maturation due to defective DNA synthesis |
| Deficiency of what two substances can cause Megaloblastic Anemia to occur? | B12 or Folic acid/Folate |
| Define Pernicious Anemia | PA is the most common megaloblastic anemia caused by B12 deficiency. Because the Vitamin B12 cannot be absorbed, metabolic function will be disrupted, causing damage to multiple organs |
| In Megaloblastic dyspoiesis, the pathophysiological affect a defiency in B12 or Folate has on the body will manifest in | defective RBC maturation |
| The most common, pharmacological cause for Folic acid deficiency is | Alcoholism |
| What is the purpose of Intrinsic Factor in relation to B12? | It binds to B12 in the stomach (forming a stable complex) and brings it into the small intestine, where it gets absorbed |
| True or false: Pernicious anemia is a nutritional deficiency caused by the failure to secrete Intrinsic Factor from the stomach | True; without functioning IF protein, the Vitamin B12-IF complex will not form, meaning that the B12 will not be absorbed |
| What is the purpose of Transcobalamin II (TCII), in relation to B12? | It is a plasma polypeptide (protein) made by the liver that binds to cobalamin, bringing it to the liver and tissue. it also aids in cell synthesis, particularly wtih reticulocytes |
| Which transport protein is responsible for binding with Cobalamin and bringing it back to the liver, for storage? | R-protein |
| How is folic acid metabolized? | It gets ingested, absorbed in the small intestines, and gets reduced so it can get delivered into tissues |
| True or false: In Megaloblastic Anemia, the Hct can be normal due to the enlarged size of the red cells | true |
| What are the typical RBC indices of Megaloblastic anemia, and what would the RBC morphology look like? | MCV/MCH increase, MCHC normal (due to the altered Hct),; macro-ovalocytes, significant aniso/poikilocytosis, cabot rings, howell-jolly bodies, basophillic stippling, metarubricytes, hypersegmented neutrophils, leukopenia, decreased N:C ratio |
| What is the purpose of the Shilling Test? | Determines whether or not impaired B12 absorption can be corrected by administering injectable IF |
| Utilizing the Shilling Test, the non-radioactive cobalamin binds to all of the B12's tissue receptors, allowing us to view cobalamin excretion in 24-hour urine. What would abnormal results look like, prompting us to perform Step 2? | less than 5% of [radioactive] cobalamin is excreted within 24 hours |
| In Step 2, IF is injected alongside B12. What result would prove that a patient has Pernicious Anemia? | 10%< excretion of Cobalamin due to a lack of IF production |
| Describe the Serum B12 folate levels in PA vs Folic acid deficiency | PA: B12 levels decrease, while Folate levels remain normal or slightly increased Folic Acid Deficiency: B12 is normal, while Folate levels decrease |
| Aside from alcoholism, what else can drastically affect folate absorption? | Drug antagonists |
| What causes hemolytic anemia? | The excessive pile up of RBCs (in blood vessel, spleen or liver), causing hemolysis at a rate that the bone marrow cannot keep up with erythropoietic replacing |
| The alteration of (blank) triggers hemolysis in the body. If this destruction of RBCs happens on mass, this will cause a Hemolytic Anemia | RBC deformable membrane |
| What type of hemolytic anemia would have schistocytes in a PBS? (Intravascular or extravascular) | Intravascular/Hereditary |
| What type of hemolytic anemia would have microspherocytes in a PBS? (Intravascular or extravascular) | Extravascular |
| True or false: Hemolytic anemia can lead to a build up of bilirubin, which would cause kidney dysfunction | false: liver dysfunction |
| What effects can Inherited Hemolytic anemia have on RBCs | Defects in Hgb molecules, compromised RBC membrane integrity, Erythrocytic enzyme defects |
| This hereditary hemolytic anemia is known for having bizarre cell shape variation, severe anemia, microcytosis, and hypochromia | Hereditary pyropoikilocytosis (HPP) |
| A decrease in plasma lipoproteins can cause defects in the RBC membrane by forming dense or spherical RBCs with spiney projections. This is known as | Acanthocytosis |
| Aside from abetalipoproteinemia, what else can cause Acanthocytosis? | Spur cell anemia |
| True or false: In Spur cell hemolytic anemia, the reticulocyte count would increase significantly (10-20%) to keep up with the RBCs being lost. | True |
| What causes Xerocytosis? | A qualitative spectrin defect that causes excessive loss in potassium, resulting in RBC shrinkage. This results in fragments and microspherocytes being seen in a PBS |
| What is the principle and interpretation of the Osmotic Fragility Test? | RBCs are put into a hypotonic, saline solution to assess the membrane's bilayer stability based on how much Hgb is released; defective membranes will lyse cells at lower saline levels |
| Describe Rh null disease | deletion of all Rh determinants, causing an increase in potassium leakage, leading to the formation of stomatocytes and spherocytes |
| This enzymatic erythropoietic defect, despite being asymptomatic, will affect the pentose-phosphate pathway by causing a buildup of Hgb to form Heinz bodies | G6PD deficiency |
| What affect would Pyruvate Kinase have on RBCs? | it decreases the amount of ATP, which will cause the RBCs to shrink due to water loss, shape deformity, and an excessively tough membrane; this ultimately results in premature hemolysis |
| What pathophysiological affect will Methemoglobin Reductase deficiency have? | Cyanosis due to methemoglobin being unable to carry oxygen to tissues |
| Which cause of hemolytic anemia will result in intravascular hemolysis that is reversible once the condition no longer exists? | Chemical/Drug/Venom-associated causes |
| What test is done to assess whether or not a person has autoantibodies that will react against RBCs coated with IgG? | Direct Antibody Test (DAT) |
| Describe Warm Autoimmune Hemolytic Anemia (AHIA) | - triggered at 37 degrees (body temp) - IgG coats the RBCs - RBCs get removed by the spleen - PBS shows spherocytosis, polychromasia, schistocytes, and nucleated RBCs |
| Describe Cold AHIA | - triggered at 4 degrees celsius - IgM coats the RBCs - if complement is activated, it is intravascular - if complement is not active, it is extravascular |
| This type of Acquired Hemolytic Anemia is caused by the repetitive mechanical impact (particularly of the feet) that cause injury to the capillary beds | March Anemia |
| What cell morphology is a hallmark for extravascular hemolytic anemia? | Spherocytes |
| What causes Paroxysmal Nocturnal Hemoglobinuria? | complement inhibitors are not coated onto some RBCs, causing them to be susceptible to agglutination upon complement activation |
| This diagnostic detection method is utilized to determine RBC sensitive to complement, pertaining to Paroxysmal Nocturnal Hemoglobinuria | Flow cytometry |
| What are some common lab findings of Paroxysmal Nocturnal Hemoglobinuria? | Hgb 6g/dL> Low MCV,MCH |
| What is the difference between Paroxysmal Nocturnal Hemoglobinuria and Paroxysmal Cold Hemoglobinuria? | P. Cold Hemoglobinuria is transient and primarily appears in children suffering from viral disorders. The released of autohemolysin causes the complement to bind to RBCs in cool temp., and activate at warm temperatures, causing biphasic hemolysis |
| What are three causes of acquired hemolytic anemia> | drug use, immune mechanisms, infectious microorganisms |
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