Pathophysiology – Anemia

Anemia
comes from the Greek word “without blood”. Its a decrease of RBC causing weakness and fatigue.

Hemolytic Anemia
removes RBC’s before their allotted time of 120 day life cycle.

Lysis
to break up

Heme
Means blood. It contains porphyrin and iron (metals). Four hemes combine with one globin

Spleen
removes RBC’s from circulation. When the spleen destroys the RBC, the hemoglobin is taken out and converted into bilirubin (colors urine and stool) which is how it is excreted from the body

Reticuloendothelial tissue
traps red blood cells after they age and destroys them. They take them out of circulation.

bone marrow
thick viscous type of fluid, tissue, fills up hollow space in diaphysis and in spongy bone. This is where RBCs, WBCs and platelets (thrombocytes) are made

Pluropotential stem cell
gives rise to all three of these cells (RBC, WBC, and platelets). When erythropoietin binds to this, it gives a signal to the stem cell to create more RBCs

Kidney
releases the hormone erythropoietin which stimulates erythropoiesis.

Recombinant DNA technology
take the DNA (gene) from own cell, get a virus to take it up, have the virus deliver it to yeast, then gene transplant will occur. This process isolates the DNA that makes erythropoietin, virus delivers it in yeast (that has human DNA to make erythropoietin). This allows you to get an injection of erythropoietin.

Chemotherapy
-Kills actively dividing cells. So many immature RBCs are killed leading to anemia. Side effects are nausea, vomiting, weakness, fatigue, hair loss and anemia. An injection of erythropoietin (Procrit, Epogen, and Epovere) is given to help with side effects and regain RBC’s . Too many RBC’s may create blood clots and may lead to heart attacks.

Methemoglobin
at the end of the 120 day life cycle, this is recognized in the RBC. It is destroyed in the spleen when the spleen recognizes that there is a sufficient amount of methemoglobin in the RBC.

Globin
is made up of 4 large polypeptide chains: 2 alpha chains and 2 beta chains.

Iron
must be consumed through food. It cannot be created by the body. It can only be stored and recycled after being consumed. It attaches to oxygen in the blood. you cannot recycle this if you lose blood.

Coenzymes
-required for hemoglobin to be made properly.
-vitamin B12 (only comes from animal sources)

Vitamin B12
– comes only from animal sources
– If this passes the stomach and moves into the intestines, its gone. The hydrochloric acid will destroy it.
– this vitamin must be absorbed into the bloodstream immediately by crossing the wall of the stomach and wall of capillary.
-intrinsic factor binds to this vitamin and pulls it across the stomach wall and capillary wall into the bloodstream.

Intrinsic factor
– binds to vitamin b12 and pulls it across the stomach wall and capillary wall into the bloodstream.
– parietal cells line the inside of the stomach and make this.
– if there is a problem creating this, an injection of Vitamin B12 will be given directly into the bloodstream.

Pernicious anemia
Lack of intrinsic factor in the body. Person would need to get injections of Vitamin B12 directly into the bloodstream. Can be a side effect of bariatric surgery because the parietal cells are cut out of the stomach during surgery resulting in no intrinsic factor.

Vitamin B12 deficiency anemia
-megaloblastic or macrocytic anemia
-When there is a decreased amount of this vitamin obtained through meat products. This vitamin is needed for the synthesis of hemoglobin. Vegetarians have this as they do not consume meat. This deficiency can be specifically called pernicious anemia when this vitamin isn’t being carried into the blood stream by the intrinsic factor

Bariatric surgery
Reduces the size of your stomach by cutting part of it out or placing a band that gives you a feeling of fullness. This helps bariatric patients to lose weight because of the feeling of fulfillment. Only a small amount of food will be able to stretch the stomach. This reduces the hunger.

Erythropoietin
hormone that creates RBC and made in the kidney

Erythropoiesis
– Pathway for maturation of RBC from the stem cell.
– Factors affecting maturation in bone marrow: vitamin B12, folic acid, formation of Hgb, trace elements
-iron metabolism

Thrombopoietin
hormone that creates platelets

Thrombus
a single blood clot

Thrombi
several blood clots

Hematopoietic tissue
makes blood

Hematopoiesis
process in creating blood

Poiesis
means “to create”

Cancellous
end of bone; spongy bone

Hgb MCH
mean (avg) corpuscular (cell) hemoglobin. This tells you the average amount of hemoglobin in each cell

Hgb MCHC
means corpuscular hemoglobin concentration.

Hct
Hematocrit. The percentage of blood cells in blood.

Hct normal % range
35%-45%

Anemia secondary to blood loss
normal value of blood is 6 liters 6,000 ml).

Acute blood loss: If you lose 1000 ml of blood or more you experience hypovolemic shock. A person can lose 500 ml of blood and be ok (i.e. donating blood)

Chronic blood loss: most common cause of iron deficiency anemia
Causes: unsuspected GI tract malignancy, slowly bleeding peptic ulcer, hemorrhages

Packed red blood cells
To increase hematocrit but not blood volume, a patient needs to receive this. This has little fluid but lots of RBCs

Whole blood
To increase blood volume in a patient, this patient must get this

MCV
Corpuscular volume: the size of a red blood cell.

Normocytes
normal sized red blood cells

Macrocyte
larger than normal RBC; MCV will be higher than normal

Microcyte
small than normal RBC; MCV will be less than normal

Microcytic anemia
an anemia with smaller than normal sized RBCs. Examples: iron deficiency

Macrocytic anemia
an anemia with larger than normal sized RBCs. Examples: vitamin B12 deficiency, pernicious anemia, folic acid anemia

Normocytic anemia
an anemia with normal sized RBC’s. Examples: aplastic anemia

Reticulocyte count
if the count is elevated, it means there is a hemolytic anemia

Reticulocyte
a RBC that still has a nucleus; when the nucleus is lost it can function as a mature RBC. When it is released into the bloodstream, it doesn’t divide any further. It turns into a RBC by losing its nucleus. During a hemolytic anemia, time is decreased. Input is increased to bring back RBC’s resulting with a strained bone marrow putting out more reticulocytes.

Aplastic anemia
a failure of hematopoiesis; you cannot produce enough RBCs, WBCs and platelets. 50% of al cases are idiopathic, 50% is caused from known exposures to radiation, chemicals or drugs. Cause can also be metabolic or toxic bone marrow suppression secondary to other diseases (i.e. chronic infection, renal failure, neoplastic disease)

Thrombocytopenia
a decrease in platelets (can’t form clots, will bleed)

Leucopenia
a decrease in WBC. Immunity is decreased; increased susceptibility to infection.

Androgens
male sex hormones; this stimulates bone marrow. sometimes, this may be given to someone who has aplastic anemia.

Sideroblastic anemia
– a microcytic and/or hypo chromic anemia
– when you don’t have enough porphyrin resulting in not making enough “heme”. MCH will be decreased. The cells do not contain enough hemoglobin to carry enough oxygen because you ran out of porphyrin.
-this can be genetic (rare, sex linked) or acquired due to overexposure to alcohol, lead, or isoniazid (used to treat TB)
– treatment: if cause is genetic –> pyridine drug; if cause is acquired –> no medicine work???

Koilonychia
nails become brittle and spoon shaped due to a severe iron deficiency after years of uncorrected iron deficiency anemia

Cheilosis
corners of mouth crack and become red and painful due to a severe iron deficiency after years of uncorrected iron deficiency

Beefy tongue
smooth, shiny, bright red tongue due to a severe iron deficiency after years of uncorrected iron deficiency anemia.

Folic acid deficiency
– This is a macrocytic anemia
– chronic alcoholism can cause this deficiency as alcohol washes out all the water soluble vitamins.
– severe deficiency of this can lead to anencephaly (when a child is born without a brain and dies immediately).

This acid helps in the synthesis in hemoglobin and is necessary for the normal function of the central nervous system.

Spherocytosis
– this is a hemolytic anemia
– autosomal dominant trait
A genetically inherited disease in which the Ca and Na pumps in the wall of the RBC’s membrane doesn’t pump out water, changing the bi-concave disks into spheres (round balls). It becomes large enough to get trapped in the spleen and therefore gets taken out of circulation before 120 days lifecycle.

Treatment: splenectomy (removing the spleen and letting the liver take on the role of the spleen. Larger cells will be able to pass through the liver letting them live longer.

G6PD Deficiency
An enzyme (glucose 6 phospho-dehydrogenase) that’s used as a preservative added to RBC’s before it goes into circulation. If there is not enough G6PD, the hemoglobin will age more quickly and be taken out of circulation before 120 days. Lack of G6PD leads to direct oxidation of hemoglobin to methemoglobin with subsequent hemolysis.
– this is a type of hemolytic anemia
– high 10% of blacks have this (usually this form is mildy expressed and not associated with chronic hemolytic anemia unless exposed to antioxidant drugs)
– G6PD trait has an increased resistance to malaria
– sulfonamides and aspirin will make this situation worse; it can aggravate it.

Sickle cell trait
a carrier of the disease but free from symptoms

Sickle cell disease
– caused by a mutation in a gene (you get what is called HgbS, instead of normal HgbA for adult hemoglobin) which causes the hemoglobin to have one amino acid out of place. One amino acid will be out of place in every RBC made in the bone marrow. The cell will crumple forcing the RBC to change shape. Within a few days of circulation, the exposure of oxygen makes the cell change into a boomerang shaped cell. (The HbgS, which is the single amino acid is substituted for another in one of the polypeptide chains leading to a sickling of RBC when oxygen tension in tissue decreases). They get caught in the spleen and get removed prematurely. By decreasing time it stresses the bone marrow to increase input. The bone marrow will eventually collapse and will result with aplastic anemia. Symptoms: anemia, pain especially in bones, joints, back (may be localized or migratory), increased susceptibility to infections, hepatosplenomegaly, cardiomegaly, sickle cell crisis that can be thrombotic or aplastic.

Aplastic crisis
all symptoms of aplastic anemia; increased susceptibility to infection

capillary
one RBC will be able to pass through at a time. When the sickle cell tries to pass, it will get stuck and a clot will begin to form. With no blood moving through, the tissue will become deprived of oxygen (ischemia)

Thrombotic crisis
painful; when clots form preventing tissue from receiving blood and oxygen. Tissue can become permanently damaged.
– increase fluid intake to push cells through capillary
– the more thrombotic crises, the more damage to tissue over time.
– heart may enlarge, kidney problems may occur, more susceptible to strokes, spleen may enlarge, and increased incidents of clots.
– people may have a shorter life span
– bone marrow may stop producing adequate amount of WBC which leads to increased susceptibility to infection.

Fetal hemoglobin
while still in the womb, the fetus has this. Shortly after birth, the body turns on the gene to create an adult version. Any child who has sickle cell is born healthy.

Hydroxyurea
medication that is a powerful chemotherapeutic agent; it can shock the bone marrow into making fetal hemoglobin. The symptoms will stop but the medicine causes side effects so it cannot be taken for a long time.

Thalessemia
-microcytic and hypochromic anemia
an inherited anemia; a genetic disorder. There is a quantity problem where the body cannot produce enough of one or the other globin polypeptide chains leading to beta thalassemia or alpha thalassemia. This can lead to hemosiderosis (deposition of iron in tissues) leading to cardiac failure

Alpha thalessimia
you produce normal alpha polypeptide chains but not enough of them to complete a hemoglobin.

Beta thalessemia
you produce normal beta polypeptide chains but not enough of them to produce a complete hemoglobin

Thalessemia major
homozygous (both genes are mutated); you have the disease. A third mortality rate during pregnancy.

Thalessemia minor
-carrier of the trait but no symptoms. Heterozygous (one normal gene, one mutated gene). However, if a woman has this and becomes pregnant, she becomes a high risk. She must be watched carefully.

M=IT
M = size of the RBC mass (in avg man = 25 x 10 which is 3% lean body mass)
I = input of new RBC from bone marrow (in avg man = 0.8% of M)
T = time representing RBC life span (120 days)

One definition of anemia is when M is below normal and is the result of either decreased I or decreased T or combination of both. Anemia can also exist if RBC are inefficient in delivery of oxygen.

Anemia secondary to bone marrow dysfunction
– Aplastic anemia
– Sideroblastic Anemia
– Iron Deficiency Anemia
– Vitamin B12 and Folic Acid Deficiency Anemias

Autologous
type of bone marrow transplant using body’s own marrow

Syngeneic
type of bone marrow transplant using marrow from identical twin

Allogenic
type of bone marrow transplant using marrow from matched donor

Iron Deficiency anemia
– a microcytic and/or hypo chromic anemia
– avg adult body has approximately 4 grams of Fe of which 3 grams is in Hgb, 500mg – 1 gram in Fe stores in liver and bone marrow and remainder stored in tissues and enzyme systems. Avg daily loss of iron is about 1.5 mg which is compensated for from diet.

Causes: blood loss, gastrointestinal (malabsorption), gynecologic, urinary tract (rare), paroxysmal nocturnal hemoglobinemia
Severe clinical manifestations: koilonychia (spoon shaped nails), cheilosis (cracked corners on lips), bright red tongue

Anemias secondary to destruction of erythrocytes (hemolytic anemias)
– Spherocytosis
– G6PD
– Sickle Cell Disease
– Thalassemia

Hemosiderosis
– an effect of thallassemia.
– This is when too much iron is deposited and building up in tissues especially in the heart tissue. This will ruin the heart tissue and the heart will begin to malfunction leading to cardiac failure
– symptoms: weak, fatigue, tissue damage, heart failure
– give iron keynoting drugs to act as a magnet to pull the iron away from the tissues.

Polycythemia
Increased RBC mass
3 types:
-relative polycythemia
-secondary polycythemia
-polycythemia vera

Relative polycythemia
Hematocrit rises because of loss of blood volume

Secondary polycythemia
results from increased erythropoietin due to increased altitude or conditions that increase hypoxia such as chroni heart and lung disease or smoking

Polycythemia vera
– when the body makes too many RBC’s in the bone marrow. It’s more than what the body needs. Hematocrit rises above normal and can be deadly. Someone with this must be put on dialysis to remove RBC’s in order to keep RBCs lower.
-plueropotential stem cells are creating too many RBC’s
-too many RBCs bumping into each other can cause platelets to bump into each other causing blood clots.
-symptoms such as fingers becoming itchy, extremities becoming cold, begin to clot off the capillaries to your fingers, and clots may damage other organs. This disease can be deadly.

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