Anemia Flashcards
What is anemia
A reduction in red blood cell count, hemoglobin content, or both.
Define Erythropoiesis
The process of production of red blood cells (erythrocytes) in the body
What hormone stimulates erythropoiesis ?
Erythropoietin ( a glycoprotein, release from the kidneys when renal O2 tension declines)
Mention two disturbances of erythropoiesis
1.Cell multiplication is inhibited because DNA synthesis is insufficient. This occurs in deficiencies of vitamin B12 or folic acid (macrocytic hyperchromic anemia). 2. Hemoglobin synthesis is impaired. This situation arises in iron deficiency, since Fe2+ is a constituent of hemoglobin (microcytic hypochromic anemia).
Deficiencies of vitamin B12 or folic acid
Macrocytic hyperchromic anemia
iron deficiency, since Fe2+ is a constituent of hemoglobin
Microcytic hypochromic anemia
General signs and symptoms of anemia
include fatigue, rapid heart- beat, shortness of breath, pale skin, dizziness, and insomnia.
Anemia can be caused by
chronic blood loss, bone marrow abnormalities, increased hemolysis, infections, malignancy, endocrine deficiencie , renal failure, and a number of other disease states.
Nutritional anemias are caused by dietary deficiencies of substances such as
iron, folic acid, and vitamin B12 (cyanocobalamin) that are necessary for nor- mal erythropoiesis.
Vitamin B12 is also known as
Cyanocobalamin
Individuals with anemia that has a genetic basis, such as sickle cell disease, can benefit from pharmacologic treatment with actions beyond nutritional supplementation, such as
hydroxyurea.
Vitamin B12 (cyanocobalamin) is produced by
bacteria; B12 generated in the colon.
Which food products are rich sources of the vitamin B12 ?
Liver, meat, fish, and milk
Hydroxycobalamin is also known as
Vitamin B12a
Deficiencies of vitamin B12 can result from
Either low dietary levels or, more commonly, poor absorption of the vitamin due to the failure of gastric parietal cells to produce intrinsic factor (as in pernicious anemia), or a loss of activity of the receptor needed for intestinal uptake of the vitamin.
Intrinsic factor is
a glycoprotein produced by the parietal cells of the stomach, and it is required for vitamin B12 absorption.
In addition to gen- eral signs and symptoms of anemia, vitamin B12 deficiency anemia may cause
tingling (pins and needles) in the hands and feet, diffi- culty walking, dementia and, in extreme cases, hallucinations, para- noia, or schizophrenia
Folate deficiency may be caused by
1) increased demand (for example, pregnancy and lacta- tion), 2) poor absorption caused by pathology of the small intestine, 3) alcoholism, or 4) treatment with drugs that are dihydrofolate reduc- tase inhibitors (for example, methotrexate, pyrimethamine, and trim- ethoprim).
A primary result of folic acid deficiency is
megaloblastic anemia (large-sized red blood cells), which is caused by diminished synthesis of purines and pyrimidines. This leads to an inability of erythropoietic tissue to make DNA and, thereby, proliferate
To avoid neurological compli-cations of vitamin B12 deficiency , it is important to
evaluate the basis of the megaloblastic anemia prior to instituting therapy. Both vitamin B12 and folate deficiency can cause similar symptom .
Folic acid is well absorbed in the
jejunum unless pathology is present. If excessive amounts of the vitamin are ingested, they are excreted in the urine and feces.
Folic Acid food products source
Leafy vegetables and liver are rich in folic acid (FA)
Causes of folic acid deficiency include:
insufficient intake, malabsorption in gastrointestinal diseases, increased requirements during preg- nancy. Antiepileptic drugs (phenytoin, primidone, phenobarbital) may de- crease FA absorption, presumably by in- hibiting the formation of monogluta- mine-FA. I
Administration of FA can mask a
vitamin B12 deficiency.
A frequent cause of iron deficiency is
chronic blood loss due to gastric/in- testinal ulcers or tumors.
Iron deficiency results in
Iron deficiency results in impaired synthesis of hemoglobin and anemia
The treatment of choice of iron deficiency (after the cause of bleeding has been found and eliminated) consists of the oral admin- istration of
Fe2+ compounds, e.g., fer- rous sulfate (daily dose 100 mg of iron equivalent to 300 mg of FeSO4, divided into multiple doses).
Iron is stored in the
intestinal mucosal cells, liver, spleen, and bone marrow as ferritin (an iron–protein complex) until needed by the body. Iron is delivered to the marrow for hemoglobin production by a trans- port protein, namely transferrin.
Iron deficiency results from
acute or chronic blood loss, from insufficient intake during periods of accel- erated growth in children, and in heavily menstruating or pregnant women. Thus, iron deficiency results from a negative iron balance due to depletion of iron stores and/or inadequate intake, culminating in hypochromic microcytic anemia (due to low iron and small-sized red blood cells).
hypochromic microcytic anemia is
due to low iron and small-sized red blood cells
In addition to general signs and symptoms of anemia, iron deficiency anemia may cause
pica (hunger for ice, dirt, paper, etc.), koilonychias (upward curvature of the finger and toe nails), and soreness and cracking at the corners of the mouth
Oral preparations of iron include
fer- rous sulfate, ferrous fumarate, ferrous gluconate, polysaccharide iron complex, and carbonyl iron formulations. Of these preparations, ferrous sulfate is the most commonly used form of iron due to its high content of elemental iron and relatively low cost. The percentage of elemental iron varies in each oral iron preparation
Parenteral formulations of iron, such as
iron dextran, sodium ferric gluconate complex, and iron sucrose,
Adverse effects of iron
Adverse effects: Gastrointestinal (GI) disturbances caused by local irritation (abdominal pain, constipation, diarrhea, etc.) and dark stools are the most common adverse effects of oral iron sup- plements. Parenteral iron formulations may be used in those who cannot tolerate oral iron. Fatal hypersensitivity and anaphylactoid reactions can occur in patients receiving parenteral iron (mainly iron dextran formulations). A test dose should be administered prior to iron dextran. Excessive iron can cause toxicities that can be reversed using chelators such as deferoxamine.
Human erythropoietin (epoetin alfa), produced by recombinant DNA technology, is effective in the treatment of ane- mia caused by
end-stage renal disease, anemia associated with human immunodeficiency virus infection, and anemia in bone mar- row disorders, anemias of prematurity, and anemias in some cancer patients.
Antacids inhibit
iron absorption. Combination with ascorbic acid (Vitamin C), for protecting Fe2+ from oxidation to Fe3+, is theoretically sound, but practically is not needed.
getting too little folate, also known as vitamin B-9, during pregnancy can cause?
spina bifida
