Glossary of Clinical Lab: Anemia
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- Common presentation of anemia
- -easy fatigability
-faintness
-palpitations
-tinitis
-glossitis
-dyspnia on exertion
-vertigo
-HA
-ulcers of buccal mucosa
- Physical signs of anemia
- -pallor
-rapid pulse
-low BP
-slight fever
-systolic murmor
- Anemia definition
- -reduced number of circulating erythroctes (RBCs)
-lowering of the concentration of hemoglobin
-reduction in hematocrit
- Primary physical defect of anemia
- -reduction in the oxygen carrying capacity of the blood resulting in hypoxia
- Anemia may indicate underlying disease such as..
- -chronic hemorrhage
-neoplasm
-chronic infection
-renal failure
- Erythron
- -composite function of all erythroid tissue in the body
-encompasses production of cells, release of cells, destruction of cells
- Earliest red cell production occurs in...
- -primative mesenchymal cells called blood islands
- Blood islands
- -primative mesenchymal cells where earliest RBC production occurs
-found in fetal yolk sac in 3rd or 4th week of embryonic life
-represent the earliest hemoglobin synthesizing cells
-migrate to liver, spleen, lymph nodes, and thymus in third month of life
- RBC production in adults occurs in..
- -medullary within the bone marrow
-mostly in flat bones (sternum, ribs, skull, vertebrae, epiphysial regions of long bones)
- RBC production occurs in extra-medullary sites...
- -before birth
-with pathological conditions after birth (reversion back to more primative cell production bc normal mechanisms are not functioning properly)
- In times of increased cell demand, hematopoiesis may develop in..
- -shafts of long bones
-e.g. individuals with chronic hemolytic disease like thalassemia or sickle cell
-may cause bone pain
- Bone marrow consists of a mixture of...
- -fat (yellow marrow)
-hematopoetic marrow (red marrow)
- Red marrow is composed of..
- -dense aggregates of cells lying alongside tiny, microscopic, open vascular spaces called sinusoids
- Within the sinusoids, RBCs develop through a series of well defined stages:
- -erythroblasts (rubriblasts)
-prorubricytes
-rubricytes
-metarubricytes
- Cell release at medullary sites
- -release cells into blood stream when they are mature
- Cell release at extramedullary sites:
- -release cells in all stages (not just mature cells)
- Presence of immature cells (RBC or WBC) in the peripheral blood indicates...
- -hematoposiesis is taking place in extra-medullary sites
-disruption in bone marrow (leukemia, or space occupying lesions such as infection, cancer, granulomas, mylofibrosis)
- Normal RBC life span
- 120 days
- hemolytic anemia
- -reduced life span of RBC
- Causes of hemolytic anemia (extrinsic damage)
- -immunological reactions (antigen antibody rxns)
-trauma (mechanical heart valves)
-physical stresses such as burns, pH changes, osmostic imbalance
-"march" (feet slamming against ground found in soldiers in WWII, marathoners)
- Causes of hemolytic anemia
(instrinic causes) - -defects in hemoglobin synthesis (thalassemia, hemoglobinopathies such as sickle cell)
-invasion by animal parasites (malaria)
-enzyme defects that may lead to poor hemoglobin synthesis
- Decrease in survival of RBC (hemolytic anemia) can effect other component of the erythron such as..
- -increase in production
-alter normal release mechanism
- Changes in the erythron due hemolytic anemia will manifest in...
- peripheral blood smear
- Types of anemias
- 1. hypochromic, microcytic
2. macrocytic
3. normocytic, normochromic
- Hypochromic microcytic anemia
- -erythrocytes do not posses sufficient hemoglobin
(tiny cells so they can't hold enough hemoglobin)
-MOST COMMON
- Common variants of hypochromic microcytic anemia
- -iron deficiency
-thalassemia syndromes
-hemoglobinopathies (e.g. sickle cell)
-sideroblastic anemia
-iron-loading anemias
-refractory anemias
- Most common form of anemia is...
- iron deficiency anemia (type of hypochromic microcytic anemia)
- macrocytic anemias
- -MCV is too big
-may have oval macrocytes or round macrocytes
- Macrocytic anemia with Oval macrocytes and tear drop poikilotosis (high MCV)
- -commonly seen in megaloblastic anemias d/t vitamin B-12 or folate deficiency
-hypersegmentation or polymorphonuclear leukocytes is common feature
- macrocytic anemia with round macrocytes
- -seen in conditions causing increase in reticulocytes or in liver disease
- Normocytic Normochromic Anemia: no poikilocytosis or polychromatophillic RBCs may indicate:
- -chronic infections
-neoplasms
-chronic renal failure
-endocrine dysfunction (hypethyroidism, hypopituitarism)
- Normocytic Normochromic Anemia: poikilocytosis and occasional polychromatophillic macrocytes may indicate:
- -disturbance of erythrocyte maturation
-leukemias (esp p drug therapy)
-myelofibrosis
-carcinoma invading the bone marrow
- Normocytic Normochromic Anemia: numerous polychromatophillic macrocytes may indicate:
- -hemolysis
-acute blood loss
- In general, normocytic normochromic anemias typically indicate
- chronic disease or bleeding
- Microcytic hypochromic anemia with lack of reticulocytes may indicate:
- -compensated blood loss
-lack of response to therapy
- Microcytic hypochromic anemia with increased reticulocytes may indicate:
- -bone marrow hyperplasia
-response to blood loss
-response to therapy
- Msot common cause of microcytic anemia is...
- iron deficiency
- Iron deficient can be ruled out if it deosn't meet the following criteria:
- -low serum iron
-high iron binding capacity
-low ferritin
- If iron deificiency is ruled out, consider..
- -thalassemia
-hemoglobinopathy (eg sickle cell)
- If thalassemia and hemoglobinopathy are ruled out, consider..
- -anemia of iron overload
-sideroblastic anemia
- Amount of iron an normal adult body contains:
- 3.0-4.0 g of iron
- Relative levels of iron in a normal adult body:
- -hemoglobin: 66%
-tissure iron: 33%
-myoglobin and cytochromes: <1%
-plasma transferrin <0.1%
- Normal plasma iron
- 100-125 ug/ml
- Normal iron binding capacity
- 300-400 ug/ml
- Normal saturation for circulating transferrin
- 1/3 saturated
- RBCs in bone marrow can extract iron from....
- plasma
- Percentage of cardiac output received by erythroid marrow
- 5% of cariac output
- Precentage of available iron extracted by erythroid marrow
- 85% of available iron (so it is very efficeint at picking up iron)
- Iron deficiency definition
- total body iron is less than normal
- Sequential stages of Iron deficiency
- 1. iron depletion
2. iron deficiency without anemia
3. overt iron deficiency
- Iron depletion
- -normal serum iron and iron binding capacity
-low bone marrow iron stores
- Iron deficiency without anemia
- -low serum iron and low iron binding capacity
-low bone marrow irons stores
-normal hemoglobin and hematrocrit
- Overt Iron deficiency
- -low serum iron and binding capacity
-absent bone marrow iron stores
-low hemoglobin and hematocrit
-microcytosis and hypochromia
- Amount of time needed to manifest anemia
- 2-4 months
- Iron Deficiency Anemia: prevalence
- -10-30% world population
-greater in woman, children, poor
- Causes of Iron Deficiency Anemia in infants and childen
- -milk anemia (prolonged breast feeding bc breast milk has low iron)
-rapid periods of growth (iron cannot meet increased needs)
-hookworm infections (parasites in intestines, chronic low grade bleeding in stool)
- Causes of Iron deficiency anemia in adults:
- -loss of blood (menstruation, pregnancy, etc)
-VERY RARELY DUE TO INADEQUATE INTAKE
- Iron lost during menstruation:
- 0.7 mg/day
- Iron lost during pregnancy in formation of placenta/fetus
- 4 mg/day
- Iron lost during hemorrhage of devlivery
- 330 mg
- Iron deficiency in adult males may inducate:
- -colon cancer
-bladder cancer
- Iron Deficiency Anemia: Sx
- -lassitude
-weakness
-easy fatiguability
-atrophic changes in tongue/corner of mouth
-atrophy of gastric mucosa (histamine-fast achlorydia)
-flattening/concavity of nails (spoon nails)
- Lab results for iron deficency: peripheral smear
- -microcytic/hypochromic
-target cells may be seen
-poikocytosis
-anisocytosis
-low reticulocyte count
-inc or norm platelets
-proliferation of erythroid cells in bone marrow (myeloid/erythroid ratio approaches 1:1)
- Administration of iron should result in...
- -immediate erythrocyte reponse
-gradual rise in hematocrit and hemoglobin
-retuculocytes in 10-15% (normally 0.5-1.5%)
-some normoblasts may be seen
- presence of target cells in microcytic hypochromic anemia suggests..
- -thalassemia
-hemoglobin problem
- Heme consist of..
- -4 pyrrole rings surrounding a ferrous iron
- Globin consists of..
- -4 polypeptide chains
-for any type of hemoglobin, there are 2 pairs of chains
- Chains for normal adult hemoglobin (Hemoglobin A1):
- -2 alpha
-2 beta
- Chains for Hemoglobin F (fetal hemoglobin)
- -2 alpha
-2 gamma
<1% of normal adult hemoglobin
- Chains for hemoglobin A2
- -2 alpha
-2 delta
2% of total adult hemoglobin
- Thalassemia definition
- -group of disorders wherein one or more of the globin chains is diminished or absent
-may effect alpha or beta chains
- Thalassemia: prevalance
- -most common in Mediterranean Basin and Orient
- Thalassemia is d/t..
- -defect in the genes leading to a decrease in the production of mRNA reponsible for the synthesis of specific polypeptide chains
- Heterozygous beta chain thalassemia
- -only involved 1 beta chain gene
-mild hypochromia and microsytosis occur
- Homozygous beta chain thalassemia
- -Cooley's anemia
-involves both genes controlling beta chain
-no hemoglobin A1 is produced
-hemoglobin F and A2 are increased (these have no beta chains)
- Heterozygous alpha thalassemia
- -homoglobin alpha chains are minimally compromised
- Homozygous alpha thalassemia
- -no alpha chains are made
-no hemoglobin A1, A2, F
- Thalassemis: Dx
- -hx of mild anemia since childhood
-microcytic hyprochromic RBCs
-target cells
-normal iron
-increase in hemoglobin A2 and F
- Suspect Hemoglobinopathies when...
- -hypochromic microcytic
-normal iron
-target cells present
-normal hemoglobin A2 and F
- Most common types on hemoglobinopathies:
- -hemoglobin S (sickle cell)
-hemoglobin C
- Hemoglobin S
- -glutamic acid is replaced by valine on the beta-chain of hemoglobin
(in normal, healthy person, glutamic acid is found on single locus on beta chain)
-2 mutant beta chains and 2 alpha chains form hemoglobin S, which polymerises under low oxygen conditions causing a distoration of RBC
- Hemoglobin C
- -abnormal hemoglobin with substitution of lysine for glutamic acid on the beta chain
-reduced plasticity of etythrocytes
- Homozygous for Sickle Cell
- -produce all hemoglobin S
- Heterzygous for Sickle Cell
- -produce some hemoglobin S and some regular hemoglobin
- Consider sideroblastic anemia if..
- -cells are hypochromic/microcytic
-normal iron
-no thalassemia
-no hemoglinopahthy
- Sideroblastic anemia
- -anemia d/t abnormal production of RBC
-caused by toxins (lead/zinc), drugs (thanol, isoniazid), nutritonal (copper or pyrodoxine deficiency)
- Causes of sideroblastic anemia
- -toxins
-vitamin deficiency
-mineral deficiency
-lymphoma
- 3 categories for normocytic normochromic anemia:
- 1. anemias d/t bone marrow failure
2. hemolytic anemia
3. refractory anemias (myelodysplastic syndrome)
- Causes of Normocytic normochromic anemia:
- -exposure to drugs or chemicals (benzene derivatives, chloramphenicol)
-exposure to radiation
-infection
-consistitutional factors
-idiopathic causes
- Examples of anemias due to bone marrow failure
- -pure red cell aplasia
-anemia of chronic renal failure
-anemia of endocrine disorders
- Pure red cell aplasia (anemia due to bone marrow failure)
- -acute
-chronic
-acquired
- Examples of anemia of endocrine disorders (anemia d/t bone marrow failure)
- -pituitary disease
-thyroid disease
-adrenal disease
-gonadal disease
- Clincal Mainfestations of hemolytic anemias:
- -increased hemoglobin catabolsim/breakdown
-decreased plasma haptoglobin
-hemoglobinemia (free hemoglobin in plasma)
- Increased hemglobin catablism from hemolytic anemia lead to..
- -elevation of unconjugated bilirubin
-increase in urine and fecal urobilinogen
- Hemoglobinurea in hemolytic anemia
- -occurs when hemoglobin in plasma exceeds 30 mg/dl
-at this concentration, the capacity of the proximal tubular cells to reabsorb free hemoglobin is exceeded so free, unbound hemoglobin is excreted in the urine (this is abnormal)
- Methalbuminemia in hemolytic anemia
- -free hemoglobin is catablized into methemoglobin
-some is transfered into albumin
- Congenital hemolytic jaundice is characterized by..
- -mild elevation of indirect bilirubin
-high-normal MCHC
-increased urobilinogen (colourless product of bilirubin reduction; part is resorbed and the rest is excreted in feces; trace amounts can be detected in urine)
-no bilirubin in urine
-negative direct antiglobulin test
-peripheral smear shows spheroctyes
-increase osmotic fragility of RBCs
-increase in reticuloctyes and erythroid hyperplasia
- Congential hemolytic jaundice
- -"hereditary spherocytosis"
-defect in membrane
-autosomal dominant
- Congeintial hemolytic jaundice: Tx
- -splenectomy
- Other conditions associated with spherocyte include:
- -acquired immunohemolytic anemia
-thermal injury
-hypophosphatemia
-chemical poisons
-certain septicemias
- Osmotic fragility test will prove...
- spherocytosis
- Other anemias due to membrane defects:
- -hereditary elliptocytosis
-hereditary stomatocytosis
-microangiopathic anemia
-paroxysmal nocternal hemogobinurea
- Hereditary Elliptocytosis
- -cigar shaped elliptical cells
-membrance defect unknown
-mild anemia
- hereditary stomatocytosis
- -"fish mouth" RBCs
-membrane defects caused by hyperpermeability to sodium
-potassium is forced out
-hemolysis is usually mild
-no improvement following splenectomy
-found inceidentally following consumption of large amts of ETOH
- Microangiopathic Anemias
- -damaged RBC appear as fragments
-helmet cells
-traingular pieces or other distorred images
- Causes of microangiopathic anemias
- -DIC
-prosthetic heart valve replacements
-long distance runners (march hemoglobinurea)
-following extensive burns
- Paroxysmal Nocternal Hemoglobinurea
- -acquired disorder wherein the RBC membrane is hypersensitive to complement
-cause is unknown, perisists for life with no cure
-platelets and WBCs may be effected
-pt presents c fatigue and low grade anemia
-reticulocytes present
-spherocytes do NOT occur
-mild respiratoty acidosis with sleep
-hemoglobinurea in a.m.
- hemolytic anemias d/t extracorpuscular defects:
- -caused by antibodies destroying the integrity of the RBCs
-acquired disorders
-positive direct antiglobin test (direct Coombs test) d/t warm or cold autoantibodies
-hemolysis is secondary to sequestration of cells in liver
- Hemolytic anemias (extracorp. defect) caused by warm antibodies
- -idiopathic acquired autoimmune hemlytic anemia
-secondary immunohemolytic anemia
- Idiopathic acquired autoimmune hemolytic anemia
- -mild to severe
-positive DAT of unknown cause
-pt shows splenomegaly, marked spherocytosis, reticulocytosis
- Secondary immunohemolytic anemia
- -develops with other disorder like neoplasma, leukemia, lupus
- Hemolytic anemias with cold antibodies
- -in association with viral disorders (esp pneumonia and mononucleosis)
-in association with lymphoproliferative disease
-idopathic cold agglutinin disease
-mild to severe anemia
- Paraxysmal Cold hemoglobinurea
- -associated with syphilis
-produced intravascular hemolysis due to exposure to cold
-antibody is known as Donath-Landsteiner antibody
- Reticulocytes
- -immature red blood cells
-develop in mature in bone marrow
- Number of reticulocytes is a good indicator of...
- -red bone marrow activity
-can be used to monitor the progress of the treatment of anemia
- Increased reticulocytes (reticulocytosis) may indicate..
- -hemolytic anemia
-sickle cell anemia
- Decresed reticulocytes may indicate...
- -chemotherapy
-aplastic anemia
-pernicious anemia
-bone marrow malignancies
-problems with erythropoitin production
-other casues of poor RBC production
- Megaloblastic anemia
- anemia resulting from deficiceny in vitamin B12 and folilc acid
- Magaloblastic anemia hematologic findings:
- -dec RBC
-dec hemoglobin
-increased MCV
-normal reticulocyte
-platelet dec or norm
-macrocytes are present (large RBC)
-ovalocytes may be present (oval shaped RBCs)
-anisocytosis
-poikilocytosis
-bone marrow shows megaloblastic hyperplasia
- anisocytosis
- increased varitaion in RBC size
- poikilocytosis
- abnormally shaped RBC
- Pernicious anemia
- -autoimmune anemia
-antibodies are directed against intrinsic factor or parietal cells that make intrinsic factor (intrinsic factor is required fo vitamin B12 absorption)
-macrocytic anemia with low vita,in B12
- Where are RBC cleared out of circulation?
- spleen
- Hemolytic anemia hematologic findings:
- -spherocytes (RBCs smaller and rounder than normal)
-increased reticulocytes
-inc bilirubin levels
-dec haptoglobin
- Bilirubin
- -yellow breakdown of normal heme catabolism
-responsible for th yellow color of bruises
-formed when RBC die and their hemoglibin is broken down within the macrophages to heme and globins
-can lead to juandice
- Haptoglobin
- -a protein in the blood plasma the binds free hemoglobin released from erythrocytes
-once bound, the haptoglobin-hemoglobin complex is removed via the spleen
-decreased with hemolytic anemia
- Aplastic anemia
- -bone marrow does not produce enough, or any, new cells to replenish the blood cells
-low RBC, low WBC, loe platelets
- Sideroblastic anemia hemotologic findings:
- -inc ferritin
-dec total iron binding capacity
- Sickle Cell disease
- -RBC change shape upon deixygenation bc of polymerization of the abnormal sickle hemoglobin (Hgb S or Hb S)
-damaged RBC can casue RBC to become stuck in blood vessels and cause obstructions (infarction, ischemia)
- Sickle cell hemotologic findings:
- -microcytic, hypochromic
-inc reticulocytes (reflecting new RBC replacing the rapidly destroyed older RBCs)
-inc WBC and platelet (often)
- Thalassemia
- -genetic defect results in synthesis of abnormal hemoglobin molecules
-as a result, blood cells are vulnerable to mechanical injury and early death