Anemia Flashcards
Normal Characteristics of RBC
▪️Round, biconcave, disc-shaped, anuclear cells
▪️About 7-9 m in diameter
▪️Central pallor occupying 1/3 of the original size
▪️Lifespan of 110-120 days
▪️Internal volume of 80-100 fL
Etiologic Classification of anemia
🔴Impaired red cell formation
➢Deficiency (iron, B12, folate)
➢Bone marrow failure
🔴Blood loss
🔴Hemolytic anemia
●Corpuscular (membrane defects, enzymatic defects, hemoglobin defects)
●Extracorpuscular (immune hemolytic anemia)
ETIOLOGIC FACTORS (iron deficiency anemia)
- Low-birth-weight neonates.
- Unusual perinatal hemorrhage.
- Blood loss ( especially in older children): occult bleeding may be caused by a peptic ulcer, Meckel diverticulum, polyp, hemangioma, inflammatory bowel disease, or hookworm infestation.
- Intense exercise conditioning, as occurs in competitive athletics in high school, may result in iron depletion in girls; this occurs less commonly in boys.
Clinical Manifestations
(iron deficiency anemia)
1- Pallor is the most important sign of iron deficiency
2- Pagophagia (the desire to ingest unusual substances such as ice or dirt)
3- irritability and anorexia
4- Tachycardia and cardiac dilation, and systolic murmurs (when the hemoglobin level falls below 5 g/dl)
5- Children with iron deficiency anemia may be obese or may be underweight
6- Neurologic and intellectual dysfunction, attention deficit, alertness, learning problems, cognitive deficits and poor school performance
7- Nail flattening and koilonychia (concave nail)
8- Sore tongues and papillary atrophy
9- Angular stomatitis (painful cracks at the angle of the mouth)
10- In young children psychomotor delay and behavioral problems
11- Poor muscle endurance, gastrointestinal dysfunction
12- impaired WBC and T cell function with recurrent infections.
Laboratory Findings
(iron deficiency anemia)
♦️The tissue iron stores (bone marrow hemosiderin) disappear
♦️ The serum ferritin falls below normal ♦️Serum iron decreases, the iron binding capacity (serum transferrin) increases
🔴Hemoglobin synthesis decreases
🔴 RBCs become smaller, mean corpuscular hemoglobin (MCH) and mean corpuscular volume (MCV) become low
🔴 microcytosis, hypochromia and increased RBC distribution width (RDW).
Microcytic anemia ddx
- Iron deficiency anemia
- Lead poisoning
- Anemia of inflammation
- Thalassemia
- Sideroblastic anemias (rare in children)
treatment (iron deficiency anemia)
🟢iron medications
🔸Oral form of ferrous salts (sulfate, gluconate, fumarate) A daily total of 4-6 mg/kg of elemental iron in three
divided doses provides an optimal amount.
🔸 A parenteral iron (iron dextran) is an effective form of iron, but it is not superior to oral iron indicated in
1)Malabsorption
2) Re-education of child and parent is not successful
3) gastrointestinal complaints secondary to oral iron (more common in adolescents).
🔊Iron medication should be continued for 8 wk after blood values are normal.
🔊Failures of iron therapy
1. non compliance
2. poorly absorbed form of iron
3. continuous unrecognized blood loss
🟢diet
The family must be educated about the patient’s diet; the consumption of milk should be limited to 500 mL/24 hr or
less to increase the amount of iron-rich foods, and reduce the blood loss from intolerance to cow’s milk proteins.
🟢Blood transfusion is indicated only when there is severe
anemia (Hb < 4g/Dl) or when superimposed infection may
interfere with the response should be given only 2-3
ml/kg of packed cells.
Responses to Iron Therapy
12-24 hr
36-48 hr
48-72 hr
4-30 days
1-3 mo
⭕️ 12-24 hr replacement of intracellular iron enzymes; subjective improvement; decreased irritability; increased appetite
⭕️36-48 hr initial bone marrow response; erythroid hyperplasia
⭕️ 48-72 hr reticulocytosis, peaking at 5-7 days (inversely proportional to the severity of the anemia)
⭕️ 4-30 days Increase in hemoglobin level (may increase as much as 0.5 g/dL/24 hr)
⭕️ 1-3 mo Repletion of stores
Folic Acid
〰️Folates are abundant in many foods, including green vegetables, fruits, and animal organs (liver, kidney).
〰️Folates are heat labile and water soluble.
〰️Folic acid is absorbed throughout the small intestine.
〰️Body stores of folate are limited, and megaloblastic anemia occurs after 2-3 mo on a folate-free diet.
Clinical Manifestations (folic acid deficiency)
🧷 peak incidence 4-7 mo of age.
🧷 Besides having the usual clinical features of anemia, affected infants with folate deficiency are
〰️irritable
〰️fail to gain weight adequately
〰️have chronic diarrhea.
Etiology (folic acid deficiency)
1️⃣Inadequate folate intake
. increased vitamin requirements (very-low-birth weight infants, chronic hemolysis).
• Goat’s milk and powdered milk are deficient with folic acid, unless supplemented.
2️⃣Decreased folate absorption
• Malabsorption (chronic diarrhea, diffuse inflammatory disease, celiac disease, and enteroenteric fistulas).
• Previous intestinal surgery.
• Certain anticonvulsant drugs (e.g., phenytoin, phenobarbital).
3️⃣congenital abnormalities in folate metabolism
4️⃣drug-induced abnormalities in folate metabolism
• methotrexate binds to dihydrofolate reductase and prevents formation of tetrahydrofolate, the active form.
• pyrimethamine (as therapy of toxoplasmosis), and trimethoprim
Laboratory Findings (folic acid deficiency)
🩸low serum folic acid level
🩸levels of RBC folate are a better indicator of chronic deficiency.
🩸macrocytic anemia (mean corpuscular volume MCV >100 fL)
🩸variations in RBC shape and size are common (RDW high)
🩸the reticulocyte count is low, neutropenia and thrombocytopenia.
🩸the neutrophils are large, some with hypersegmented nuclei.
🩸 serum activity of lactate dehydrogenase (LDH) is markedly elevated.
🩸Bone marrow:
➰hypercellular
➰erythroid hyperplasia
➰megaloblastic changes
➰Large, abnormal neutrophilic forms
(giant metamyelocytes)
➰cytoplasmic vacuolation are
seen, as well as hypersegmentation of the nuclei of megakaryocytes.
Treatment (folic acid deficiency)
🟢Folic acid (0.5-1 mg/day) for 3-4 wk until a definite hematologic response has occurred.
🟢 If the specific diagnosis is in doubt, smaller doses of folate (0.1 mg/day) may be used for a week as a diagnostic test,
because a hematologic response can be expected within 72 hr.
🟢Larger doses of folate can correct the anemia of vitamin B12 deficiency but may aggravate the neurologic abnormalities.
🟢Transfusions are indicated only in severe anemia, or very sick child.
Vitamin B12 (Cobalamin)
🔹 Vitamin B12 is present in animal food.
🔹The cobalamins are released in the acidity of the stomach and combine intrinsic factor (IF), and are absorbed in the distal ileum via specific receptors for IF-cobalamin.
🔹 In the plasma, cobalamin binds to transcobalamin II, which carries the vitamin B12 to the liver and bone marrow.
🔹 Older children and adults have sufficient vitamin B12 stores to last 3-5 yr.
However, in young infants born to mothers with low vitamin B12 stores (breast fed infants of vegans mothers or having pernicious anemia), clinical signs of cobalamin deficiency can become apparent in the first 4-5 mo of life.
Etiology (vitamin B12 deficiency)
1️⃣ Inadequate vitamin B12 intake
♾️ It may occur in strict vegetarians or vegans.
2️⃣ Lack of intrinsic factor
♾️ Congenital pernicious anemia (rare autosomal recessive disorder due to an inability to secrete gastric IF or secretion
of functionally abnormal IF It differs from the typical disease in adults in that the stomach secretes acid normally and is histologically normal. There are no antibodies to parietal cells and no associated endocrine disorders. The symptoms of juvenile pernicious anemia become prominent at around 1 yr of age.
♾️ Gastric surgery
3️⃣ Impaired vitamin B12 absorption ♾️Inflammatory diseases (regional enteritis)
♾️ Surgically removed terminal ileum
♾️ An overgrowth of intestinal bacteria (diverticula or duplications of the small intestine) may cause consumption of B12; appropriate antibiotic therapy is
effective.
♾️fish tapeworm (Diphyllobothrium latum).
♾️ Rarely, familial defect of the receptor for IF-B12 in the terminal ileum.
4️⃣ Absence of vitamin B12 transport protein
