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Average size of an RBC



Average amount of hgb in an average RBC



Average concentration of hgb per unit of volume in an average RBC.



Too large RBCs



Normal size RBCs



Too small RBCs



Normal amount of hgb. Aside: Hemoglobin A is the normal hgb.



Too little hgb, diseased. No such thing as too much hgb!



New (young) RBCs, elevated when RBC production increases as the bone marrow compensates for RBC shortage.


Anemia & causes

Abnormally low hgb in blood. Causes: decreased RBCs, decreased hgb, or both. HGB, HCT, and RBC usually move together in a lab assessment.


Anemia s/s

chronic fatigue, SOB, pallor (of skin or oral or conjunctival mucosa), increased HR and RR, syncope, coma


Steps of anemia diagnosis

Step 1. CBC with red cell indices. Step 2. Determine if the anemia is associated with a) failed bone marrow production of RBCs (not enough cells or hgb) versus b) RBC loss either by hemorrhage or destruction. A reticulocyte count should be 0% in failed production and >2.5% in RBC destruction.



impairs hgb synthesis, so iron deficient RBCs contain less hgb than normal. The RBCs are hypochromic (pale) & low MCHC (small). Pretty unique to IDA


Acute blood loss anemia

main threat is shock or death. The volume of lost RBCs is initially replaced by water and albumin synthesis by the liver, and the patient develops a temporary dilutional anemia until the marrow can replace RBCs.


Dilutional anemia

-healthy RBCs with normal size and hgb content
-increased number of reticulocytes. -The RBCs are normocytic and normochromic (normal MCV and MCHC)


Chronic blood loss anemia

-usually occurs in abnormal menstrual bleeding and intestinal bleeding. Intestinal bleeding is usually slow, and new RBCs from marrow replace lost blood.
-In rapid intestinal blood loss, the lack of RBCs in the vascular space is made up by fluid and the patient initially develops a dilutional anemia until the bleeding stops. And then, oral iron replacement is not absorbed in the intestines and cannot make up for lost RBCs so the patient develops IDA.



Premature destruction of RBCs


Features of hemolytic anemia

-short RBC life span,
-active, hypercellular bone marrow (as marrow works overtime to replace dying cells),
-increased blood erythropoietin (as kidneys secrete more to stimulate RBC production),
-blood that contains a high count of new RBCs (reticulocytes – on microscopic exam these are blue)


Hemolytic anemia s/s

enlarged spleen (splenomegaly), increased free hgb in plasma (hemoglobinemia), dark urine due to hgb in urine (hemoglobinuria), jaundice


Hereditary spherocytosis

genetic disorder of structural protein (spectrin) in red cell membrane that renders cells stiff and spherical rather than flexible and biconcave, so they are unable to successfully pass through the spleen, leading to splenic destruction.


Hereditary spherocytosis s/s

anemia, jaundice, splenomegaly.


Glucose-6-phosphate dehydrogenase (G6PD) deficiency

X-linked recessive genetic disorder. G6PD is important in the supply of energy to stabilize the red cell membrane, so without it, RBCs are fragile and easily destroyed. Patients are subject to acute hemolytic episodes upon exposure to oxidizing drugs, toxins, or infections. Disproportionately affects black men


g6pd s/s

same as hemolytic anemia. enlarged spleen, free hgb, dark urine, jaundice


Sickle cell anemia

a kind of hemoglobinopathy, a fam of autosomal recessive genetic disorders of hemoglobin synthesis. The hgb is molecularly defective, unstable and causes hemolysis. Caused by hemoglobin S. Disproportionately affects AAs


Sickle cell anemia patho

In hgb S valine is substituted for glutamic acid in the 6th amino acid of the beta globin chain of hgb. Oxygenated Hgb S is less soluble than oxygenated hgb A, so at sites with low oxygen on RBCs, a gel is formed that deforms RBCs into a sickle shape. This subjects cells to hemolysis as they pass through the spleen. They also plug arterioles and capillaries leading to infarction & thrombosis. Also leads to bone deformaties d/t chronic compensatory marrow hyperactivity.


Sickle cell anemia s/s

s/s: Evident shortly after birth as anemia with hemolysis. Skeletal deformities, hepatosplenomegaly that leads to spleen shrinking from infarcts.
-obstruction of small vessels: ischemia, infarction, gangrene
-anemia: causing high output heart failure and cardiomegaly, bone marrow hyperplasia, bone deformities d/t overactive bone marrow
-hemolysis: pigment gall stones from bilirubin secretory overload
-infection: caused by loss of splenic immune fxn (hyposplenism), or from pathogens born out of tissue necrosis. Others: Salmonella bone infections, pneumococcal sepsis, parovirus leading to marrow failure


Sickle cell crisis

Acute severe abd pain and bone pain caused by vascular occlusions usually brought on by low oxygenation as in increased altitude, infection, dehydration, acidosis. 50% survival to mid-life


Thalessemias (in general)

Inherited microcytic anemias (low MCV). Inherited in Mendelian fashion. Mediterranean and SE azn ppl.


Thalassemia pathology

Impairs synthesis of alpha or beta polypeptide chains of the globin of hgb. Affects the amount (not the structure) of the hgb synthesized. Makes RBC membrane fragile and easily hemolyzed. RBCs pale and small d/t low hgb cytoplasm


Beta Thalassemia (2 kinds)

Decreased production of beta globin. Inherited.


Beta thalassemia minor (heterozygous)

Mild anemia, asymptomatic.


Beta thalassemia major cases (homozygous)

severe. Pts die before 20y/o. Severe microcytic, hypochromic hemolytic anemia. RBCs look like “target cells.” Jaundice, splenomegaly, hyperactive bone marrow, bone deformities. Liver and spleen enlarge (myeloid metaplasia) to produce more RBCs. Iron overload (hemochromatosis) caused by repeated transfusions


Alpha thalassemia

Decreased production of alpha globin. Inherited. Vary from mild & asymptomatic to severe fetal anemia and IUFD.


Immune hemolytic anemia (2 kinds!):

-Warm antibodies (IgG): most active at normal body temp., s/s anemia, common splenomegaly. Tx: withdrawal of drug and corticosteroids
-Cold antibodies (IgM): most active at low temps and precipitated by exposure to cold – air, drinking cold fluid, washing with cold water. s/s: back or leg pain, fever, vomiting, diarrhea, hemoglobinuria. Tx: avoid cold


Immune hemolytic anemia causes

caused by antibodies directed against antigens on the RBC membrane, this leads to premature removal by the spleen. Occurs in association with other autoimmune diseases (esp. lupus), WBC malignancies, mononucleosis and mycoplasma pneumoniae, reactions to certain hapten drugs,


Mechanical hemolytic anemia

caused my shredding of RBCs as they pass through mechanical devices such as artificial heart valves. Also caused by autoimmune vasculitis or DIC because the RBCs have to fit through tiny or occluded vessels and shred.



Most common nutritional deficiency globally. It is a symptom; there is always an associated underlying condition. Commonly blood loss via menstruation or GI bleeding, poor iron absorption, or increased need of normal development. Breastmilk to low in iron so infants are at risk. Assume the cause of IDA in men and post-menopausal women is GI malignancy. In non-developed nations GI bleeding is caused by intestinal worms. -TIBC high, low plasma iron, low ferritin, low percent saturation of transferrin. RBCs are small (microcytic, low MCV) & pale (hypochromic, low MCHC). Low reticulocyte


IDA patho

Hinders the ability of bone marrow to make hgb. Average western diet is sufficient for men but not for menstruating women. Decreased reserve in pregnancy.



Iron-protein complex found in bone marrow, liver, spleen, skeletal muscle. Plasma ferritin is a good indicator. Transported throughout body by transferrin (made in liver)


Total iron binding capacity

how total transferrin is measured, but is theoretical. The actual value is called “percent saturation of TIBC”


IDA diagnosis

Thalassemia also causes microcytic, hypochromic RBCs but in thalassemia the bone marrow pours out fresh RBCs, which can be documented by high reticulocyte count. In IDA, reticulocyte count is low


Megaloblastic anemia

Anemia associated with a B12 (cobalamin) or folic acid deficiency are characterized by macrocytic red cells. Their bone marrow precursors are unusually large (hence “mega”). Macrocytic RBCs (high MCV), low WBC (leukopenia), and low plt (thrombocytopenia), low reticulocyte count, low plasma b12 and folate. Bone studies will reveal hypercellular marrow filled with megaloblastic red and white cell precursors.


Megaloblastic anemia patho

2 and folic acid are necessary for DNA synthesis, so a deficiency would lead to a decrease in RBC production in the bone marrow. Because DNA synthesis is impaired, RNA synthesis continues but makes fewer and they’re huge.


Intrinsic factor

A protein secreted by gastric mucosa that is necessary for b12 intestinal absorption. Causes of insufficient b12 absorption: gastrectomy, ileum resection, IBS


Pernicious anemia

autoimmune disease featuring autoantibodies against the gastric mucosal linings (parietal cells) that produce IF. Caused by chronic atrophic gastritis. Used to be very fatal!


B12 deficiency can lead to neuro damage!

peripheral neuropathy, dementia, subacute combined degeneration (decreased position sense, vibration sensation in extremities, weakness, spasticity, ataxia). Folate deficiencies do not affect the nervous system.


anemia of chronic disease

Second to IDA worldwide. “Bone marrow does not expand appropriately to the anemia”. Caused by -RBC survival shortened -erythropoiesis impaired, -iron reutilization is impaired. Usually caused by neoplasms, chronic infections, autoimmune disorders. Inflammatory mediators interfere with the mechanism that transports iron from iron storage into RBC production. Iron stores (Ferritin) increases even as RBCs starve for iron. s/s: those of anemia and then those of underlying disease. CLUE: Increased bone marrow iron stores and low transferrin rule out IDA.


Aplastic anemia

Primary failure of ALL marrow elements – RBCs, WBCs, megakaryocytes. Usually presents as anemia. Can lead to hemorrhage (plt decr.) and infection (wbc decr.). Can be caused by drugs causing toxic effect on bone marrow. Many times it is idiosyncratic (the toxic effect is disproportionate to the dose)


Aplastic anemia

Primary failure of ALL marrow elements – RBCs, WBCs, megakaryocytes. Usually presents as anemia. Can lead to hemorrhage (plt decr.) and infection (wbc decr.). Can be caused by drugs causing toxic effect on bone marrow. Many times it is idiosyncratic (the toxic effect is disproportionate to the dose)


aplastic anemia s/s

normal anemia symptoms & low plt, petechiae, ecchymoses, internal bleeding, low wbc counts (granulocytopenia) leading to infections. Bone marrow biopsy shows hypocellular bone marrow that is mostly fat. Tx: HORSE anti-thymocyte globulin, bone marrow transpl.


Myelophthisic anemia:

rimary myelophthisic anemia is marrow fibrosis of unknown cause and is rare. Linked to sarcoidosis, TB, others. Marrow may be displaced in some diseases like Gaucher disease. Most commonly caused by marrow displacement by metastatic cancer (breast and prostate). White cells non-deformed but are released early in their life cycle.


Extramedullary hematopoiesis or myeloid metaplasia

As marrow fails, spleen and liver enlarge to compensate RBC production



Replacement of marrow by malignancy or fibrosis


Myelophthisic anemia s/s slash diagnosis

Hepatosplenomegaly, normochromic, normocytic anemia, nucleated RBCs and immature WBCs, confirmed by bone marrow biopsy. Primary myelofibrosis: no treatment exists


Viruses of Respiratory tract