Causes of anemia

1. Iron deficiency (hypochromic, microcytic): the most common cause of anemia in the US. Look for low iron/ferritin level, elevated total iron-binding capacity (TIBC; also known as transferrin), and lowTIBC saturation. Rarely patients have a.craving for ice or dirt (pica) or Plummer-Vinson syndrome (esophageal web producing dysphagia, iron deficiency anemia, and glossitis). In a patient over 40, rule out colon cancer as a cause of chronic: blood loss. Iron deficiency anemia is common in women of reproductive age because of menstrual irregularities. Give iron supplements to all infants except full-term infants who are exclusively breast-fed; giving cow's milk before 1 year of age may cause anemia through GI bleeding. Start iron supplementation at 4 6 months for full-term infants and at 2 months for preterm infants. Iron supplements also are commonly given during pregnancy and. lactation because of increased demand. To treat iron deficiency anemia, correct: the underlying cause if possible and treat with oral iron supplementation for roughly 6 months.

2. Folate deficiency (macrocytic): commonly seen in alcoholics and pregnant women. All women of reproductive age should take folate supplements to prevent neural tube defects. Rare causes include poor diet (e.g., tea and toast), methotrexate, prolonged course of trimethoprim/sulfamethoxazole, anticonvulsant therapy (especially phenytoin), and malabsorption. Look for macrocytes and hypersegmented neutrophils (even one should make you think of the diagnosis) and low folate levels (serum or RBC). Treat with oral folate.

3. Vitamin B)2 deficiency (macrocytic): most commonly due to pernicious anemia (antiparietal cell antibodies). Remember the physiology ofBJ2 absorption and the association with vitiligo and hypothyroidism. Other causes include gastrectomy, terminal ileum resection, diet (strict vegan), chronic pancreatitis, and Diphyllobothiium latum (fish tapeworm) infection. Peripheral smear looks the same as in folate deficiency (macrocytes, hypersegmented neutrophils), but the patient has neurologic deficiencies (loss of sensation or position sense, paresthesias, ataxia, spasticity, hypcrreflexia, positive Babinskt sign, de mentia). Look for low serum B13 , achlorhydria (no stomach add secretion, elevated stomach pH), and antibodies to parietal cells. A Schilling test usually determines the etiology. Usual replacement route is intramuscular, because most patients cannot absorb Bl2.

4. Thalassemia (microcytic, hypochromic): must be differentiated from iron deficiency. Iron levels are normal in thalassemia; iron is contraindicated because it may cause overload. Look for elevated hemoglobin A, (p-thalassemia only) or hemoglobin F (J3-thalassemia only), target cells, nucleated RBCs, diffuse basophilia on peripheral smears, x-ray of the skull showing a "crew-cut" appearance, splenomegaly, and positive family history (more common in blacks, Mediterraneans, Asians). No treatment is required for minor thalassemia; patients often are asymptomatic as they are used to living at a lower level of hemoglobin and hematocrit. Thalassemia major is more dramatic and severe. Treat with as-needed transfusions and iron chelation therapy to prevent hemochromatosis. Diagnosis is made by hemoglobin electrophoresis. There are four gene loci for alpha-chain and only two for beta -chain thalassemia. Alpha thalassemia is symptomatic at birth, or the fetus dies in utero (hydrops); beta thalassemia is not symptomatic until 6 months of age.

5. Sickle cell anemia: smear gives it away. Look for very high percentage of reticulocytes. Sickle cell anemia almost always is seen in blacks (8% are lieterozygotes in U.S.). Watch for classic manifestations of sickle cell disease-.

■ Aplastic crises (due to parvovirus BI9 infection)

■ Bone pain (due to microinfarets; the classic example is avascular necrosis of the femoral head)

■ Dactylitis (hand-foot .syndrome; know what it looks like)

■ Renal papillary necrosis

« Splenic sequestration crisis

■ Autosplenectomy (increased infections with encapsulated bugs)

■ Acute chest syndrome (mimics pneumonia)

■ Pigment cholelithiasis

Diagnosis is made by hemoglobin, electrophoresis. Screening is done at birth, but symptoms usually do not appear until around 6 months of age because of lack of adult hemoglobin production.Treat with prophylactic penicillin (start as soon as the diagnosis is made), proper vaccination (including pneumococcal vaccine at the age of 2 years old), folate supplementation, early treatment of infections, and proper hydration. Sickle crisis is characterized by severe pain in various sites due to R.BC sickling. Treat with oxygen, lots of IV fluids, and analgesics (do not be afraid to use narcotics). Consider transfusions if symptoms and/or findings are severe.

6. Acute blood loss (normocytic, normochromic): immediately after blood loss, hemo globin and hematocrit are normal; it takes at least 3-4 hours (often more) for reetprili bration. Look for pale, cold skin; tachycardia; and hypotension. Transfuse if indicated, even with normal hemoglobin and hematocrit in the acute setting.

1. Autoimmune hemolytic anemia (normocytic, normochromic)-—can have multiple etiologies: lupus (or meds that cause lupus, like procainamide, hydralazine, and isoniazid), drugs (classic is methyldopa, also PCN/cephalosporins/sulfas and quinidine), leukeinia/lymphoma or infection (classic is Mycoplasma, also EBV and syphilis). Coombs' test is positive, may have spberocytes due to incomplete macrophage destruction in ex travascular hemoly si s

8. Lead poisoning (hypochromic, microcytic): classically seen in children. With acute poisoning, look for vomiting, ataxia, colicky abdominal pain, irritability (aggressive, behavioral regression), and encephalopathy, cerebral edema, or seizures. Usually, however, poisoning is chronic and low-level; look for pica (especially paint chips and dust in old buildings, which may still have lead paint); residence in an old or neglected building; residence near a lead-smelting or battery-recycling plant; family members who work at such plants; basophilic stippling; and elevated free erythrocyte protoporphyrin (FEP). Screening asymptomatic children for serum lead level at 1 and 2 years of age is important (screen at 6 months if risk factors are present) because chronic low-level lead exposure may lead to permanent neurologic sequelae. Screen and mea sure symptomatic lead exposure with serum lead levels (should be < 10 |lg/dl). Treat with decreased lead exposure (best and first treatment) as well as as-needed lead chelation therapy (succimer in children, dimercaprol in adults; in severe cases, use dimercaproJ plus edetate for children or adults).

9. Sideroblastic anemia (microcytic, hypochromic): increased or normal iron, ferritin, andTIBC saturation (which distinguish it from iron deficiency), polychromatophilic stippling, and the classic "ringed sideroblast" in the bone marrow (know what it looks like). Sideroblastic anemia may be related to myelodysplasia or future blood dyscrasia. Manage supportively; in rare cases the anemia responds to pyridoxine. Do not give iron!

10. Anemia of chronic disease (microcytic, hypochromic, or normocytic): look for diseases that cause chronic inflammation (rheumatoid arthritis, lupus erythematosus, cancer, tuberculosis). Serum iron is low, but so isTJBC (thus, the % saturation may be nearly normal). Serum ferritin is elevated (because ferritin is an acute-phase reactant, the level should be increased).Treat the underlying disorder to correct the anemia. Do not give iron!

11. Spherocytosis (normochromic): look for spherocytes, family history (autosomal domi nant), splenomegaly, positive osmotic fragility test, and increased mean corpuscular hemoglobin concentration.Treatment often involves splenectomy. Spherocytes also may be seen in extravascular hemolysis, but the osmotic fragility test is normal.

12. Chronic renal disease: the kidney produces erythropoietin; thus, you may give erythropoietin in end-stage renal disease to correct the anemia.

11 Aplastic anemia: usually idiopathic; may be caused by chemotherapy, radiation, malignancy (especially leukernias), benzene, and medications (chloramphenicol, carba-mazepine, phenylbutazone, sulfa drugs, zidovudine, and gold). Look for decreased white blood cells and platelets to accompany anemia. Stop any possible causative medication; then try antithymocyte globulin or bone marrow transplant.

14. Myelophthisic anemia: usually due to myelodysplasia/myelofibrosis or malignant invasion and destruction of bone marrow (most common cause). Look for marked anisocy-tosis (different size), poikilocytosis (different shape), nucleated RBCs, giant and/or bizarre-looking platelets, and teardrop-shaped RBCs on the peripheral smear. A bone-marrow biopsy is usually done and may reveal no cells ("dry tap" because marrow is fi-brotic) or malignant-looking cells.

15. G-6-PD deficiency: X-linked recessive (males affected); most common in. blacks and Mediterraneans. Look for sudden hemolysis or anemia after fava bean or drug exposure (antimalarials, salicylates, sulfa drugs), or after infection or diabetic ketoacidosis. Heinz bodies and bite cells also are seen on peripheral smear. Diagnosis is made with RBC enzyme assay. Do not perform the assay immediately after hemolysis—you may get a false-negative result because all of the older RBCs already have been destroyed and the younger RBCs are not affected.Treat by avoiding precipitating foods and medications. Discontinue the triggering medication first!

16. Other causes: endocrine failure (especially pituitary and thyroid); mechanical valves (which hemolyze RBCs); disseminated intravascular coagulation, thrombotic thrombocytopenic purpura, and hemolytic uremic syndrome (look for schislocytes/RBC fragments and appropriate other findings); other hemoglobinopathies (hemoglobins C and I! fairly common); paroxysmal nocturnal or cold hemoglobinuria; Clostridium perfringens, malaria, babesiosis, and hypersplenism (always accompanied by splenomegaly and often by low platelets and white blood cells).

Transfusions: always based on clinical grounds.Treat the patient, not the lab value; there is no such thing as a "trigger value" for transfusion. Different blood components have different indications:

1. Whole blood; used only for rapid, massive blood loss or exchange transfusions (poisoning, thrombotic thrombocytopenic purpura)

2. Packed RBCs: used instead of whole blood when the patient needs a transfusion

3. Washed RBCs; free of traces of plasma, whtie blood cells, and platelets; good for IgA deficiency and allergic or previously sensitized patients

4. Platelets: given for symptomatic thrombocytopenia (usually < l0,000/|Ul)

5. Granulocytes: rarely used for neutropenia with sepsis caused by chemotherapy

6. Fresh, frozen plasma: contains all clotting factors; used for bleeding diathesis when one cannot wait for vitamin K to take effect (disseminated intravascular coagulation, severe warfarin poisoning) or vitamin K will not work (liver failure).

1. Cry «precipitate: contains fibrinogen and factor 8; used in hemophilia, von Willebrand disease, and disseminated intravascular coagulation

The most common cause of Mood transfusion reaction is lab error, "type O negative can be used when you cannot wait for blood typing or the blood bank does not have the patient's type. If a transfusion reaction occurs, the first step is to stop the transfusion! Look for febrile reaction (chills, fever, headache, back pain) from antibodies to white blood cells; hemolytic reaction

(anxiety, discomfort, dyspnea, cliest pain, shock, jaundice) from antibodies to RBCs; or allergic reaction (urticaria, edema, dizziness, dyspnea, wheezing, anaphylaxis) to an unknown component in the donor serum. Patients with associated oliguria should be treated with IV fluids and diuresis (mannitol or furosemide). Massive transfusions may lead to bleeding diathesis from thrombocytopenia (look for oozing from puncture/IV sites) and citrate (calcium chelator). Patients also may develop hyperkalemia.

Disseminated intravascular coagulation (DIC): most commonly due to pregnancy and obstetric complications (50%), malignancy (33%), sepsis, and trauma (especially head trauma, prostate surgery, and snake bites). DIC usually manifests as bleeding diathesis. Look for the classic oozing/bleeding from puncture or IV sites, but patients may have thrombotic tendencies. Look for prolonged prothrombin time (PT), parital thromboplastin time (PIT), and bleeding time (BT); positive D-dimer and increased .fibrin degradation products; thrombocytopenia; and decreases in fibrin and clotting factors (including factor 8, which is normal in hepatic necrosis).Treat the underlying cause (evacuate uterus, give antibiotics). Patients may need transfusions, fresh frozen plasma, or, rarely, heparin (only in the presence of thrombosis).

Eosinophilia: causes include idiopathic etiology, allergy, eczema, atopy, angioedema, drug reactions, parasitic infections, blood dyscrasias (especially lymphoma), to filer's syndrome (pulmonary eosinophilia), autoimmune diseases (e.g., lupus erythematosus, rheumatoid arthritis, inflammatory bowel disease), IgA deficiency, and adrenal insufficiency.

Basophilia: think of allergies, neoplasm, or blood dyscrasia.

Bleeding problems: lupus anticoagulant .may cause a prolonged PTT but the patient has a tendency toward thrombosis. Look for associated lupus, positive Venereal Disease Research Laboratory or rapid plasma reagin test for syphilis, and/or history of miscarriages. Deficiencies in protein C, protein S, or antithrombin Hi also may cause increased tendency toward thrombosis. Patients are treated with anticoagulant therapy to prevent deep venous thrombosis, pulmonary embolism, and other complications.

Clotting tests: PT for extrinsic system (prolonged by warfarin), PTT for intrinsic system (prolonged by heparin), and BT for platelet function:

■':■.■"''.'■.■ P&ATEJLET '-.-■iUiC' DJSfcAStK . PT ". " PTT - , BT ■ NO.'.. _ OTHHU. - '

■" von Witle.bMiici ' Normal '. High'. ■'■ "High ■ Normal Normal "■' Autosomal.dominant (look for family history).'

;.'H«nophUfe"A/B "Normal- ■; High ■" Normal-■' Normal'' : Normal . '•'••• rX-ltakeSiWfesitfveiA »'tow-fkttir'S?

.■ inc. ■■ H«gh High J Ugh low. ■■ ■Nomial/lcfvv- ' Appiropriate. history, taw factor, ^' level -- ■':./,.;■■ .

liver'1 laihire \ V': High'' .-■ "' High: :: ■ ."Normal \ NomM/iewr_'\Nom»al/low; '•Jaondice/.rtorra»lfet^8.feyelrdb iwt gh^Yitaifito Kf-'

Heparin .'" Ni.u trial ■ High' .' tfomul ■' Normal/low- ;'£ionniti.-". ' .-Watch fps: thrombocytopenia, thipnibosis '..

■ Waifariii-■"'■ ■ ■'■ High :N<winaT Normal.1 ■ Normal. Normal Vitamin K antagonia (factorf, t, and 10) ■. . . '. .ITS;- Normal Normal. :Hlgh .' Low'" ■; -.. Normal.'... -Watchforprflcedijig.npper'respira^ ■

■ TTP.: ;i|oonal. ^fifarsaal--"- High-.-. - .• ...-$«»9;' '.■■' Low .. 'Heuatiyds.{sitte<ir)>i^'symptoias;treatw(th-.-

' plawiuphereisiis;'do net give'platelet«;.;

•Si iu vy .' Nominal ■ '■'.Normal'■'.; Normal: 'Normal"' ■ Normal ■'" FitigernaH, gum', arid bone' hemorrhages ■ .

■ PIC s disseminated, intravascular coagulation, ftp a idioikathic.thxotnbo'cytopeiiic purpura, TTF . ~ thrombotic dumihaeytopjshic pur-piira^CN^^-central ncrvOTis sysfenj-. ' -

Thrombocytopenia may be caused by idiopathic thrombocytopenic purprua, thrombotic thrombocytopenic purpura, hemolytic uremic syndrome, disseminated intravascular coagulation,

HIV, splenic sequestration, heparin (treat by first stopping heparin), other medications (especially quinidine and sulfa drugs), autoimmune disease, and alcohol. Bleeding from thrombocytopenia is in the form of petechiae, nose bleeds, and easy bruising.

Note: Do not give platelets to a patient with thrombotic thrombocytopenic purpura or heparin-associated thrombocytopenia. They may cause thrombosis.

Vitamin C deficiency (scurvy) may cause bleeding similar to that seen with low platelets (splinter and gum hemorrhages, petechiae); perifollicular and subperiosteal hemorrhages are unique to scurvy. Patients have a poor dietary history (the classic example is hot dogs and soda), myalgias and arthralgias, and capillary fragility. Bleeding is due to collagen problems in vessels. Treat with oral vitamin C.

Bleeding tendency also may be due to inherited connective tissue disorder (Ehlers Danlos syndrome, Marfan syndrome, pseudoxanthoma elasticum, osteogenesis imperfecta) or chronic steroid use, but it is rarely a clinical problem.


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Cancer Sta tistics (See table, top of next page) Important points:

1. In children and younger adults, leukemia is the most common cancer. Remember, how ever, thai age has the most significant impact on the incidence and mortality rale of cancer.

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