Anemias Flashcards
WBC
4.5-10.5
RBC
3.7-5.4
Hemoglobin
12-16
Hematocrit
35-48%
MCV
78-100. Mean corpuscular volume. The average size of the RBC. (micro/normo/macrocytic)
MCH
27-34. Mean cell hemoglobin. (normo vs. hypochromic)
MCHC
31-37. Mean cell hemoglobin concentration.
RDW
11.5-14.5% Measure of the variation in size.
Platelets
150-450.
Reticulocytes
1-2%. “lots of blue mean lots of new” on peripheral smear. Indication of the bone marrow’s RBC production. Usually mature within 1-2 days.
Anisocytosis
Large variation in RBC size
Poikilocytosis
abnormally shaped RBCs
Symptoms of anemia
Usually occur when Hb is less than 7. fatigue, weakness, lightheadedness, syncope, dyspnea, palpitations
Signs of anemia
Pallor, tachycardia, bounding pulse, orthostatic changes, GI blood loss, High output heart failure and shock.
Microcytic Hypochromic anemias
Iron deficiency, thalassemias, sideroblastic.
Normocytic normochromic anemias
Hypothyroidism, liver disease, chronic disease (can be micro and/or hypo).
Macrocytic (megaloblastic) anemias
folate and B12 deficiency.
Most common cause of anemia
Iron deficiency
Iron Deficiency Anemia etiology
menstruation, pregnancy, GI bleed, decreased iron absorption (celiacs, bariatric surgery, H.pylori infection).
Iron Deficiency Anemia Classification
Microcytic Hypochromic
Iron Deficiency Anemia MCV
Decreased
Iron Deficiency Anemia RDW
increased
Iron Deficiency Anemia Ferritin
Decreased less than 12
Iron Deficiency Anemia TIBC
Increased
Iron Deficiency Anemia manifestations
Glossitis, cheilitis, Koilonychia, pica, dysphagia (esophageal webs/plummer-vinson syndrome), restless leg syndrome.
Iron Deficiency Anemia treatment
Determine the underlying cause (colonoscopy and/or radiographic testing), replace iron stores
Thalassemia definition
Inherited disorder. Reduction in the synthesis of the globin chains of Hb.
Alpha Thalassemia classifications
1=silent carrier
2=Trait. Mild microcytic anemia
3=hemolytic anemia
4=hydrops fetalis
Beta Thalassemia classifications
Minor (trait): dysfunction of one beta chain. asymptomatic micro/hypo anemia
Major (Cooley anemia): Dysfunction of both beta chains. Usually die before 30.
Thalassemia MCV
Extremely LOW (60-75)
Thalassemia classification
microcytic hypochromic.
Thalassemia RDW
normal
Thalassemia serum Fe
Normal to elevated
Thalassemia Ferritin
Normal to elevated
Thalassemia TIBC
decreased
Thalassemia peripheral smear
Poikilocytosis, target cell, nucleated RBC.
Thalassemia electrophoresis
Is Diagnostic.
Thalassemia treatment
folic acid supplementation. If severe: regular transfusions or splenectomy. Severe beta Thalassemia: hematopoietic cell transplant.
Anemia of chronic disease
Seen in the elderly, chronic inflammation and organ failure. Due to abnormal iron metabolism, impaired EPO production etc.
Anemia of Chronic Disease MCV
Normal
Anemia of Chronic Disease classification
Normocytic normochromic
Anemia of Chronic Disease ferririn
normal or increased
Anemia of Chronic Disease serum Fe
variable. low with chronic inflammation
Anemia of Chronic Disease TIBC
variable. low with chronic inflammation.
Anemia of Chronic Disease treatment
Treat the underlying condition. EPO may be beneficial. refer.
Myelodysplastic syndrome definition
acquired disorder of hematopoietic stem cells causing dysplastic and ineffective RBC production. Group of underlying conditions. Can progress to marrow failure or leukemia.
Myelodysplastic syndrome etiology
idiopathic or secondary to an exposure (radiation etc)
Sideroblastic Anemia Etiology
Usually myelodysplastic syndrome. Can be hereditary. Alcoholism, lead poisoning, medication, chronic infection/inflammation.
Sideroblastic Anemia definition
abnormal RBC iron metabolism, diminished heme synthesis, bone marrow produces ring sideroblasts.
Sideroblasts
Nucleated RBC precursors that contain iron. Granulocytes filled with iron.
Sideroblastic Anemia MCV
varies
Sideroblastic Anemia Hct
Moderate (20-30%)
Sideroblastic Anemia ferritin
Normal or elevated
Sideroblastic Anemia peripheral smear
anisocytosis and poikilocytosis
Sideroblastic Anemia bone marrow biopsy
Ring sideroblasts is diagnostic
Sideroblastic Anemia treatment
discontinue the med, treat the infection/inflammation, pyridoxine (vitamin B6) if hereditary. refer.
Normocytic Normochromic with increased reticulocytes
Prior/recent hemorrhage or recent hemolysis.
Normocytic Normochromic with normal reticulocytes and normal bone marrow
anemia of chronic disease, hypothyroidism, liver disease.
Normocytic Normochromic with normal reticulocytes and abnormal bone marrow
Myelofibrosis, luekemia, myeloma, mestastases and renal failure.
Mactocytic anemias
MCV >100. Megaloblastics (folate and B12 deficiency), acute hemorrhage, hemolysis.
Megaloblastic anemias
Folate and B12 deficiency. Impaired DNA sythesis results in disorderd RBC maturation resulting in large RBC. Have to differentiate between the two. Untreated B12 deficiency can lead to subacute combined degeneration of the spinal cord.
Vitamin B12 deficiency symptoms
glossitis, jaundice, splenomegaly, decreased vibratory sense and proprioception. Paresthesia, ataxia, confusion and dementia.
Vitamin B12 metabolism
Only available in the diet. Binds intrinsic factor (from gastric parietal cells) in the stomach. In the ileum B12 is released from IF and absorbed.
Pernicious anemia
Deficiency of intrinsic factor due to autoimmunity (parietal cells), gastrectomy, ileal disease/resection, bacterial overgrowth or intestinal parasite.
Vitamin B12 deficiency MCV
elevated >100
Vitamin B12 deficiency peripheral smear
hypersegmented neutrophils, anisocytosis, poikilocytosis, macro-ovalcytes.
Schilling test
Vitamin B12 deficiency. tests for autoantibodies to IF.
Vitamin B12 deficiency methylmalonic acid
elevated
Vitamin B12 deficiency homocysteine
elevated.
Vitamin B12 deficiency Treatment
Parenteral vitamin B12. Daily IM of 1,000 micrograms for a week then weekly for a month then monthly for life.
Folic Acid metabolism
Available in the diet but has a short half life (3 weeks) so the body stores are small. Deprivation for 4-5 months can result in anema.
Folic Acid Deficiency etiology
alcoholism, end of pregnancy, anticonvulstant therapy, malabsorption syndrome, hemolytic anemias.
Folic Acid Deficiency MCV
elevated >100
Folic Acid Deficiency peripheral smear
hypersegmented neutrophils, anisocytosis, poikilocytosis, macro-ovalcytes.
Folic Acid Deficiency methylmalonic acid
Normal
Folic Acid Deficiency homocysteine
elevated.
Folic Acid Deficiency treatement
treat the underlying cause. Replacement 1mg daily or 5mg daily for malabsorption.
Hemolytic anemia
Destruction of RBC. Marrow can’t compensate for survival time of less than 20 days
Hemolytic anemia symptoms
jaundice, gallstones (bilirubin), increased risk of salmonella and pneumococcus infections.
Hemolytic anemia reticulocytes
elevated
Hemolytic anemia peripheral smear
immature RBC, nucleated RBC, schistocytes (RBC fragments).
Hemolytic anemia Unconjugated bili
increased
Hemolytic anemia LDH
elevated.
Hemolytic anemia Hb
increased
Serum haptoglobin
mucoprotein produced in the liver that binds Hb released from lysed RBC. Bound haptoglobin is then catabolized by the spleen.
Hemolytic anemia serum haptoglobin
decreased with intravascular hemolysis.
Intravascular hemolysis causes
Fragmentation: either traumatic/macroangiopathic (prosthetic heart valve) or microangiopathic from fibrin strands in the vessels. Enzyme deficiency (G6PD) or paroxysmal nocturnal hemoglobinuria.
Extravascular hemolysis causes
hereditary spherocytosis, sickle cell, autoimmune hemolytic anemia, incompatible blood transfusion, drug induced.
Hereditary Spherocytosis
autosomal dominant disease with mild hemolytic anemia. RBC become easily trapped in the spleen and destroyed
Hereditary Spherocytosis peripheral smear
Dense globular appearance with lack of central pallor
Hereditary Spherocytosis MCV
normal
Hereditary Spherocytosis symptoms
often asymptomatic, mild jaundice, splenomegaly, can develop megaloblastic anemia (need more folate).
Hereditary Spherocytosis diagnosis
osmotic fragility test. Cells hemolyze in a hypotonic fluid.
Hereditary Spherocytosis treatment
spleenectomy. Increased risk of infection so wait until adulthood and give pneumococcal vaccine.
Sickle Cell anemia
Autosomal reccessive disorder of Hb structure. African american population. RBC becomes sickle shaped when deoxygenated.
Sickle Cell anemia symptoms
usually begin at 4-6 months. Delayed growth/development, increased infections. Symptoms are worsened by dehydration, hypoxia, altitude and exercise.
Sickle Cell anemia Symptoms are caused by:
chronic hemolysis (aplastic crisis, bilirubin gallstones), vaso-occlusive ischemic tissues (pain crisis, osteonecrosis, CV incidents, MI, splenic infacrts, leg ulcers.
Sickle Cell anemia classification
normochromic normocytic
Sickle Cell anemia Hb
5-11
Sickle Cell anemia reticulocytes
elevated 10-20%
Sickle Cell anemia peripheral smear
sickled RBC, nucleated RBC, target cells, Howell-jolly bodies, thrombocytosis.
Sickle Cell anemia diagnosis
screen with sickledex and Hb electrophoresis reveals HbS
Autoimmune hemolytic anemia peripheral smear
polychromasia, spherocytosis, nucleated RBC
Autoimmune hemolytic anemia treatmen
ID the cause, corticosteroids, splenectomy, folic acid supplementation.
Incompatible blood transfusion diagnosis
coombs test detects antibodies coating the transfused RBC.
Aplastic anemia etiology
acquired abnormality of bone marrow stem cells. Idiopathic, chemical/drug exposure, viral illness, ionizing radiation. Pancytopenia is hallmark.
Aplastic anemia bone marrow
absence of precursor cells.
Aplastic anemia symptoms
weakness, infections, bleeding.
Aplastic anemia treatment
Refer to hematology. Blood component replacement, bone marrow transplant, immunosuppressants.
Iron deficiency treatment iron stores
Ferrous sulfate 325mg BID-TID until corrected then an additional 3-6 months. Parenteral iron may be needed in select patients as well as possible blood transfusions.