Pathophysiology of Anemia and Polycythemia

Body fluid loss but not an increase in erythrocytes, such as dehydration from heavy sweating or profuse diarrhea.

Blood Loss Anemia, Aplastic Anemia, Megaloblastic Anemia, Hemolytic Anemia

Exercise greatly increases tissue demand for oxygen, leading to extreme tissue hypoxia and potentially acute cardiac failure.

An increase in hematocrit leads to an increase in blood viscosity, which increases the resistance to blood flow.

The mother's anti-Rh antibodies will cross the placenta and cause hemolysis of the Rh-positive fetal RBCs, leading to Erythroblastosis Fetalis.

Symptoms include tachycardia, palpitations, cardiomegaly (if chronic), and eventually heart failure and death.

Mean Corpuscular Hemoglobin.

Iron overload due to repeated transfusions.

Infection, chemical exposure to medication, and certain foods.

Microcytic anemia.

Because the number of erythrocytes does not increase.

Decreased rate of erythropoiesis, excessive losses of erythrocytes, and deficiency in the hemoglobin content of erythrocytes.

Abnormal hemoglobin, specifically hemoglobin S (HbS).

When they unload oxygen or when oxygen levels are lower than normal, such as during vigorous exercise.

In a few weeks.

Because the rate of iron absorbed by the intestines to form hemoglobin is much slower than hemoglobin losses, resulting in smaller erythrocytes with too little hemoglobin.

The erythropoietin mechanism is triggered after blood removal, causing the RBCs to be quickly replaced.

Hyperchromic anemia.

Normocytic anemia.

Increased RBCs lead to increased blood viscosity, causing sluggish blood flow and plugged capillaries, which decreases O2 delivery to tissues.

Vitamin B12 and folic acid.

The heart is not capable of pumping much greater quantities of blood than it is already pumping.

Hemolytic Anemia

The afterload on the heart increases, and the heart must work harder to maintain adequate blood flow to the tissues.

They block blood flow through small vessels, leading to tissue damage.

Valine is substituted for glutamic acid at position six of the beta chain.

Mean Corpuscular Hemoglobin Concentration.

Hematocrit levels can increase from 45% to 65%.

Macrocytic anemia.

Hematocrit levels in primary polycythemia can be as high as 70-80%.

Low MCV (Mean Corpuscular Volume).

Increased cardiac output will partially counterbalance the reduced oxygen-carrying effect of anemia by increasing the rate of blood flow, delivering almost normal quantities of oxygen to the tissues.

Megaloblastic Anemia

It causes difficulties for blood to flow through the arteries, veins, and capillaries.

A condition where RBCs are very small and spherical rather than being biconcave discs, making them fragile and easily ruptured.

Excessive X-ray treatment, certain industrial chemicals (e.g., benzene, insecticides), and certain drugs (e.g., cytotoxic drugs like chloramphenicol, indomethacin).

3 to 6 weeks.

Blood doping is the practice of increasing the number of red blood cells (RBCs) to enhance athletic performance, particularly in aerobic events, because it causes polycythemia.

Reinfusing stored blood causes temporary polycythemia, increasing the oxygen-carrying capacity due to higher hematocrit, which leads to greater endurance and speed.

Normochromic anemia.

The normal range of RBC is 5 x 10^6 cells/mm³.

Normal MCV (Mean Corpuscular Volume).

Blood Loss Anemia

The Rh-negative mother gets sensitized with RBCs of an Rh-positive fetus at delivery and forms anti-Rh antibodies.

The increased blood pressure required to maintain adequate flow may damage blood vessels.

Exposure to Rh-positive fetal red blood cells during delivery.

They are much smaller than normal and have too little hemoglobin, leading to microcytic, hypochromic anemia.

Hemoglobin is changed into met-hemoglobin, which inhibits oxygen binding.

The normal hematocrit range is 42-45%.

The downside is an increase in blood viscosity.

High MCV (Mean Corpuscular Volume).

Deficiency in intrinsic factor (pernicious anemia), or vitamin B12 and/or folic acid.

Pernicious anemia.

A normal number of erythrocytes is simply concentrated in a smaller plasma volume.

The erythrocytes grow too large, with odd shapes, and are called megaloblasts.

Fatigue, pale skin, shortness of breath, and feeling chilly.

Erythroblasts cannot proliferate rapidly enough to form normal numbers of RBCs, resulting in erythrocytes that are mostly oversized with abnormal shapes and fragile membranes.

Lack of functioning bone marrow.

An impairment of all formed elements.

Anemia resulting from rapid blood loss, such as from a severe stab wound.

It decreases resistance to blood flow, allowing greater than normal quantities of blood to flow through the tissues and return to the heart.

A condition where one of the globin chains is absent or faulty, leading to thin, delicate erythrocytes deficient in hemoglobin.

Mean Corpuscular Volume.

Dehydration during long races can cause the blood to further concentrate, becoming thick and sticky, which can lead to clotting, stroke, and heart failure.

Primary polycythemia is caused by a tumor-like condition of the bone marrow, leading to increased erythropoiesis.

Secondary polycythemia is an appropriate EPO-induced adaptive mechanism to improve O2 carrying capacity and delivery to tissues.

Aplastic Anemia

Because they become fragile and cannot resist compression forces, especially as they go through the capillaries and the spleen.

A hemolytic disease of the newborn caused by the mother's anti-Rh antibodies attacking the Rh-positive red blood cells of the fetus.

Spherocytes are very small and spherical, whereas normal RBCs are biconcave discs.

Anti-Rh antibodies from the mother cross the placenta and attack the Rh-positive red blood cells of the fetus, causing hemolysis.

Peripheral tissue vasodilation.

According to which hemoglobin chain is affected (α, β).

The G6PD/NADPH pathway.

Polycythemia is a condition characterized by an increased number of blood cells.

Because O2 delivery is already more than adequate with normal RBC numbers.

These erythrocytes rupture easily, leaving the person in dreadful need of an adequate number of red cells.

The lifespan of erythrocytes is short because they are destroyed faster than they are produced, leading to serious anemia.

Exposure to gamma ray radiation from a nuclear bomb blast.

1 to 3 days.

Cardiac output increases to a very high level, 3-4 times higher than normal.

A quantitative problem of too few globins synthesized.

A hereditary abnormality in the activity of glucose-6-phosphate dehydrogenase, an important enzyme in RBC metabolism.

Hypochromic anemia.

Abnormalities of the erythrocytes, which can be hereditary or acquired, causing RBCs to become fragile and rupture easily.

A change in just one of the 146 amino acids in the β chain of the globin molecule.

The blood concentration of RBCs.

Because they are fragile and cannot resist compression forces, especially as they go through the capillaries and the spleen.

Slight but persistent blood loss, such as from a bleeding ulcer or excessive menstruations in females.

Athletes may receive injections of erythropoietin (EPO) or have their RBCs drawn off and reinjected a few days before events.

Macrocytes, Normocytes, and Microcytes.

The intake of fava beans and various drugs (e.g., antimalarial drugs, NSAIDs).

They link together to form stiff rods, making hemoglobin S spiky and sharp.

It decreases to as low as 1.5 times that of water, compared to the normal value of about 3.

Because they are fragile and prone to rupture as they travel through the narrow splenic capillaries.

Greatly increased cardiac output and increased pumping workload on the heart.

Hyperchromic, Normochromic, and Hypochromic.

Blood doping is considered unethical and is banned because it provides an unfair advantage and poses significant health risks.

In primary polycythemia, the RBC count can reach 11 x 10^6 cells/mm³.

In secondary polycythemia, the RBC count can reach 6-8 x 10^6 cells/mm³.

Secondary polycythemia occurs in people living at high altitudes or in patients with chronic lung diseases or cardiac failure.

Deficiency of hemoglobin in the blood, caused by either too few RBCs or too little hemoglobin in RBCs.

A reduction below normal in the O2-carrying capacity of the blood and low hematocrit.