hematology Flashcards
(157 cards)
1
Q
hematology
A
study of blood (and blood forming tissues) and its components
2
Q
what is the hematologic system made up of
A
blood, bone marrow, the spleen, and lymphatic system
3
Q
what is blood responsible for
A
transport of metabolic components, nutrients, hormones, gas exchange, immune defense, and coagulation
4
Q
what is total blood volume in adults
A
5.5 L
5
Q
two major groups of plasma proteins
A
albumins and globulins
6
Q
what are the cellular elements of blood
A
rbc (erythrocytes), WBC (leukocytes), and platelets (thrombocytes)
7
Q
what are erythrocytes responsible for
A
tissue oxygenation
8
Q
which is the most abundant cells in blood
A
erythrocytes
9
Q
what are leukocytes responsible for
A
defend body against infection and remove dead or injured host cells
10
Q
what are thrombocytes responsible for
A
blood coagulation and control of bleeding
11
Q
classifications of leukocytes
A
agranular- lymphocytes and monocytes
granular- eosinophils, basophils, neutrophils
12
Q
what is the site of residence, proliferation, differentiation, or function of lymphocytes and mononuclear phagocytes
A
lymphoid organs
13
Q
what is the largest lymphoid organ
A
spleen
14
Q
role of spleen
A
at site of fetal hematopoiesis, filters and cleanses blood and acts as a reservoir for lymphocytes and other blood cells
15
Q
what is the site of development or activity of large numbers of lymphocytes, monocytes and macrophages
A
lymph nodes
16
Q
lymph nodes are the site of development or activity of what
A
lymphocytes, monocytes, and macrophages
17
Q
what does the bone marrow consist of
A
red (active or hematopoietic) marrow and yellow (inactive marrow)
18
Q
what cells does bone marrow contain
A
stem cells
19
Q
two mc stem cells
A
hematopoietic and mesenchymal
20
Q
what do hematopoietic stem cells develop into
A
blood cells and osteoclasts
21
Q
what do mesenchymal stem cells develop into
A
adipocytes, chondrocytes, fibroblasts, osteoblasts, and other stromal cells
22
Q
what do osteoblasts and osteoclasts produce
A
cytokines that affect proliferation and maintenance of hematopoietic cells
23
Q
myelopoiesis
A
development of granulocytes (neutrophils, eosinophils, and basophils) and monocytes from the differentiate of myeloid progenitor cells in the bone marrow
24
Q
granulocytes are released
A
to blood and stored
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monocytes are released to
blood and travel to various tissues to become tissue macrophages and dendritic cells
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lymphocytes are degenerated from ..... in a process called ...
lymphoid progenitor cells, lymphopoiesis
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lymphocytes are released
into blood stream to undergo further maturation in primary and secondary lymphoid organs
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platelets develop from ... in a process called ...
megakaryocytes, thrombopoiesis
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thrombopoiesis is controlled by what
thrombopoietin
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what happens during thrombopoeisis
megakaryocytes undergo mitosis but not cell division and the cytoplasm and plasma membrane fragment into platelets
31
what does lymphoid progenitor form
B cell, T cells, and natural killer
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what do myeloid progenitors make
mast cells, reticulocytes, megakarocyte, and myeloblast
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reticulocyte form
erythrocyte
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megakaryocytes form
thrombocytes
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myeloblast form
basophil, eosinophil, neutrophil, and monocyte
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monocytes form
dendritic cells and macrophage`1
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specific hematopoietic growth factors (colony stimulating factors)
adequate production of myeloid, erythroid, lymphoid, and megakaryocytic lineages
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hematopoiesis occurs where
liver and spleen of a fetus and in bone marrow after birth
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hematopoiesis
blood cell production
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erythropoiesis
development of rbcs
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regulation of erythropoiesis is mediated by what
erythropoietin
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what is erythropoietin secreted by
kidneys
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why is erythropoietin secreted
in response to tissue hypoxia
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what does erythropoietin cause
a compensatory increase in erythrocyte production if the oxygen content of the blood decreases because of anemia, high altitude or pulmonary disease
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what vitamins does erythropoiesis need
vitamin b12, folate, b6, riboflavin, niacin, and others
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the iron cycle reutilizes iron from where
from old or damaged erythrocytes
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what does iron bind to in the blood
transferrin
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iron is transported to what
marcophages
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where is iron stored and what is it stored as
in the cytoplasm as ferritin
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what is iron homeostasis controlled by
hepcidin
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what is hepcidin
a small hormone produced by hepatocytes that controls iron homeostasis which regulates ferroportin
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what is ferroportion
principle transport of iron from stores in hepatocytes and macrophages from intestinal cells that absorb dietary iron
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primary homeostasis
1. vasoconstriction
| 2. formation of platelet plug
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secondary homeostasis
3. activation of clotting (coagulation) cascade
| 4. formation of fibrin blood clot
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what is fibrinolysis
clot retraction and clot dissolution
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what is the function of the fibrinolytic system
lysis of blood clots
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what splits fibrin and fibrinogen into fibrin degradation productions that dissolve the clot
plasmin (an enzyme)
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life span of rbc
120 days
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what do rbcs contain
hemoglobin
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what is hemoglobin
protein that transports oxygen
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abcs size and shape
uniform but may be affected by variety of conditions like B12 deficiency, folate deficiency, and iron deficiency
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what stimulates the bone marrow to produce a high number to neutrophils
infection
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what WBC is increased with allergies
eosinophils
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what rapidly multiples in leukemia
abnormal (immature or mature) wbcs
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what is essential for blood clotting
platelets
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what do platelets release
chemical signals that attract and promote clumping of additional platelets
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if pt has condition that causes low platelets (thrombocytopenia) what may they have
bleeding and bruising
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if a pt has too many platelets (thrombocytosis) what can it cause
excessive clotting
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what is cbc
tests that evaluate cells that circulate in blood such as rbc, wbc, and platelets
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what can cbc detect
infection, anemia, leukemia
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rbc count
actual number of rbcs in blood sample
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hemoglobin
total number of oxygen carrying protein in the blood, which generally reflects number of rbcs in the blood
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hematocrit
measure percentage of total blood volume that consist of rbcs
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mean corpuscular volume (mcv)
measurement of the average size of rbcs
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mean corpuscular hemoglobin (mch)
calculated measurement of average amount of hemoglobin inside rbcs
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mean corpuscular hemoglobin concentration (mchc)
calculated measurement of average concentration of hemoglobin inside your rbcs
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red cell distribution width (rdw)
measurement of variation in size of rbcs
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reticulocyte count
measurement of absolute count or percentage of newly released, young rbcs
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wbc count
total number on wbcs
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wbc differential
identifies and counts number of five different types of wbcs present. absolute count or percentage of total
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platelet count
number of platelets in blood
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what may or may not be included in a cbc
mean platelet volume (mpv)
| platelet distribution width (pdw)
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mean platelet volume (mpv)
measurement of average size of platelets
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platelet distribution width (pdw)
reflects how uniform platelets are in size
85
immature granulocytes (ig)
wbcs that haven't fully developed before being released from bone marrow into blood. only present in bone marrow so their presence can indicate infection or blood cancer
86
reticulocyte hemoglobin
measures the hemoglobin present inside of reticulocytes. Often reported as a Mean reticulocyte Hemoglobin Content (CHr) or a Reticulocyte Hemoglobin Equivalent (Ret-He).
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when to get blood smear
follow up to abnormal results on cbc
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what does blood smear do
compares wbc size, shape and general appearance to normal wbcs
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rbc morphology
evaluates size, shape, and color (indicator of hemoglobin content)
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Intrinsic pathway and test
8, 9, 11, ,12 --> aPTT
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extrinsic pathway and test
7 --> PT
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Anemia
A reduction in the total number of erythrocytes in circulating blood. This occurs from either a decrease in the quantity or quality of hemoglobin.
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Anemia commonly results from
```
Blood loss (acute or chronic)
Impaired erythrocyte, heme or globin production
Increased erythrocyte destruction (hemolytic anemia)
```
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Anemia from blood loss often caused by
trauma and the ensuing posthemorrhagic anemia.
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Anemia from chronic blood loss occurs
if the loss is greater than the replacement capacity of the bone marrow.
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A decrease in Hgb to less than 12 g/dL stimulates
increased production of erythropoietin.
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what is necessary for erythrocyte production
iron
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how is iron provided
iron recycled from red cell breakdown and reticuloendothelial iron stores
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The transferrin-iron complex then binds to
transferrin receptors on the surface of erythroid precursors.
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When the amount of iron on transferrin is reduced,
both hemoglobin synthesis and the proliferative response of erythroid precursors to erythropoietin are inhibited.
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The main alteration of anemia
reduced oxygen-carrying capacity of the blood resulting in tissue hypoxia.
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A reduction in the number of blood cells in the blood causes
reduction in the consistency and volume of blood.
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Initial compensation for cellular loss
movement of interstitial fluid into the blood, causing an increase in plasma volume which maintains the blood volume, but the viscosity of the blood decreases.
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The “thinner” blood flows faster and more turbulently than normal blood, causing
a hyperdynamic circulatory state.
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hyperdynamic circulatory state creates
cardiovascular changes - increased stroke volume and heart rate which lead to cardiac dilation and heart valve insufficiency if the underlying anemic condition is not corrected.
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Tissue hypoxia causes
rate and depth of breathing to increase in an effort to increase o2 availability and is accompanied by an increase in the release of oxygen from hemoglobin.
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All of these compensatory mechanism may cause
individuals to experience shortness of breath, a rapid and pounding heartbeat, dizziness and fatigue.
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In mild, chronic cases of anemia, these symptoms may be present only when there is an
increased demand for O2 (physical exertion) but in severe cases, symptoms may occur at rest.
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The skin, mucous membranes, lips, nail beds and conjunctivae become either
pain because of reduced hemoglobin concentration or yellowish (jaundiced) because of accumulation of end products of red cell destruction.
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anemia mechanism
impaired synthesis and increased destruction
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inherited impaired synthesis
Thalassemia (defect affecting erythroblast maturation)
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NUTRITION DEFICIENCIES
| impaired synthesis
B12 & Folate (deficiency affecting DNA synthesis)
Iron (deficiency affecting hemoglobin synthesis)
Anemia of chronic disease (inflammation-mediated)
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inherited increased rbc destruction
```
Hereditary spherocytosis (RBC membrane disorder)
G6PD deficiency (enzyme deficiency)
Thalassemia (deficient globin synthesis)
Sickle Cell (structurally abnormal globins - aka - hemoglobinopathies)
```
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acquired rbc destruction
Paroxysmal Nocturnal Hemoglobinuria (deficiency of glycoproteins)
Hemolytic disease of the newborn, transfusion reactions (antibody-mediated destruction)
Hemolytic uremic syndrome, DIC, thrombotic thrombocytopenia purpura (microangiopathic hemolytic anemia)
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Anemias are most commonly classified based by
morphology
116
morphology anemia
changes that affect the cell’s size (-cytic)and hemoglobin content (-chromic)
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MCV <80 fl
microcytic
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Normocytic MCV
80-100 fl
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microcytic MCV
>100 fl
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Macrocytic megaloblastic anemias are characterized by
usually large stem cells (megaloblasts) in the marrow that mature into very large erythrocytes (macrocytic).
121
Microcytic anemias have abnormally
small erythrocytes that contain unusually reduced amounts of hemoglobin.
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Microcytic include anemias that are the result of
decreased iron availability (iron deficiency anemia, anemia of chronic disease).
decreased heme production (lead poisoning, sideroblastic anemia).
decreased globin production (thalassemias, hemoglobinopathies).
123
The three most common microcytic anemias are
Iron deficiency anemia (IDA)
Thalassemias
Early anemia of chronic disease
Lead poisoning (not as common, but should be in DDx)
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iron deficiency anemia (IDA)
Usually microcytic, hypochromic
| Most common cause of anemia worldwide.
125
iron deficiency anemia (IDA) etiologies
Dietary deficiency of iron
Impaired absorption of iron (Celiac dz, bariatric surgery)
Increased requirement for iron (children, pregnant women, breastfeeding women)
Chronic blood loss (excessive menstruation, occult GI blood loss [cancer], hookworms
126
MCC in the US of iron deficiency anemia (IDA)
Chronic blood loss** (excessive menstruation, occult GI blood loss [cancer], hookworms)
127
IDA occurs when
iron stores are depleted
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iron stores are depleted when
the demand for iron exceeds the supply and develops slowly through three overlapping stages.
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Stage 1 IDA
Decreased bone marrow iron stores (hemoglobin and serum iron remain normal)
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Stage 2 IDA
Iron transportation to bone marrow is diminished, resulting in iron-deficient cells erythropoiesis.
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Stage 3 IDA
the small, hemoglobin-deficient cells enter the circulation to replace normal, old erythrocytes. This is when symptoms occur.
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Anemia of chronic disease
Usually normocytic-normochromic, but can eventually become microcytic and hypochromic
Mild to moderate anemia
Develops after 1-2 months of disease activity
Common in hospitalized patients and elderly
133
Anemia of chronic disease results from
Decreased erythrocyte life span
Suppressed production of erythropoietin (from cytokines)
Ineffective bone marrow response to erythropoietin
Altered iron metabolism -> hepcidin is an acute phase reactant that blocks the release of iron from macrophages & reduces GI absorption & ferritin is an acute phase reactant that sequesters iron into storage.
134
Hepcidin
blocks the release of iron from macrophages
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Thalassemias are caused by
mutations in the genes that code for hemoglobin. Without hemoglobin, the RBCs become SMALLER.
But the iron levels will be normal.
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Lead interferes with
enzymatic steps in the heme production pathway. As a result, there is decreased hemoglobin synthesis and microcytosis.
137
While the MCV will be microcytic in lead poisoning
actual iron levels will be normal or increased.
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The heme that is unable to be formed in lead poisoning leaves
fragments of RNA behind, which causes basophilic stippling on blood smear. (BUT, lead poisoning is not the ONLY thing that causes basophilic stippling.
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INCREASED RBC LOSS
| normocytic anemia
Acute hemorrhage
| Hemolysis
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DECREASED RBC PRODUCTION
| normocytic anemia
Bone marrow failure
Aplastic Anemia
Anemia of Chronic Disease (ACD)
141
One of the first things you want to order when a patient has normocytic anemia is a
RETICULOCYTE COUNT. WHY? Will it be high or low with each of these?
A reticulocyte count helps to determine the number and/or percentage of reticulocytes in the blood and is a reflection of recent bone marrow function or activity. indicator of the ability of a person’s bone marrow to adequately produce red blood cells (erythropoiesis).
High w/ Increased rbc loss
Low w/ decreased rbc production
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how to check for evidence of hemolysis
peripheral smear
143
Megaloblastic
Abnormal DNA synthesis, usually due deficiency in B12 or folate
Results in delayed nuclear development, causing LARGER cells
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Non-Megaloblastic
```
Mechanism not well defined
Increase in membrane lipids
DNA synthesis is NOT impaired
Causes include:
Excess alcohol consumption
Liver disease
Aplastic anemia
Myeloma
Drugs
Chemotherapy
```
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The synthesis of DNA requires
Homocysteine -> Methionine
Synthesis of Thymidine Triphosphate
This step requires Vitamin B12 and folic acid
If step 2 can’t be completed because of a B12 or folic acid deficiency, it results in:
Impaired DNA synthesis
Delayed cell division
BUT hemoglobin synthesis is normal (but the hemoglobin DNA is altered)
146
Deficiency of B12 can be caused by
Decreased intake
Vegan
Malabsorption: CELIAC disease, lymphomas, absent or antibodies to intrinsic factor, parasite infection
147
Deficiency of folate can be caused by
Poor diet (no veggies)
Alcoholism
Malabsorption: CELIAC disease, malignancy
148
Macrocytic, megaloblastic anemia caused by a lack of intrinsic factor is also called
PERNICIOUS (deadly) ANEMIA
149
The peripheral blood smear of a patient with megaloblastic macrocytic anemia will typically ALSO show
hypersegmented neutrophils with 5 or more lobes (4 lobes is normal) due to the slowed DNA synthesis.
150
Serum Iron
= the total amount of iron in the blood - nearly all of which is bound to transferrin
151
Ferritin
Measures the level of ferritin, a protein made by almost all cells in response to increased iron. The ferritin level reflects the total body iron. It will be LOW when there is iron deficiency and HIGH when there is too much iron.
152
Transferrin saturation
Dividing the iron concentration by the TIBC produces an estimate of how many transferrin iron binding sites are currently occupied. Under normal circumstances, transferrin is about 1/3 saturated and 2/3 is held in reserve.
153
Transferrin
directly measures the level of transferrin in the blood, but is dependent on the patient’s nutritional status, inflammation, etc. so it is not as widely used.
154
Total Iron Binding Capacity (TIBC)
measures the blood’s capacity to bind iron with transferrin, so it’s an indirect measurement of TRANSFERRIN.
155
IDA tests
```
MCV
Serum Iron
Ferritin
Transferrin saturation
Transferrin
Total Iron Binding Capacity (TIBC)
```
156
Serum iron level (SI)
measure of the amount of iron bound to transferrin. The proliferative capacity of the erythroid marrow and its ability to synthesize hemoglobin are functions of the serum iron level.
Normal = 50-150 ug/dL
When the SI falls below 50 ug/dL, new red blood cells will be poorly hemoglobinized.
157
Why is TIBC important
TIBC changes independently of the serum iron in situations of iron deficiency. Although TIBC declines in patients with anemia of chronic disease (inflammation), it typically increases in excess of 360 ug/dL in patients with severe iron deficiency.
The TIBC is also used to calculate a percent saturation of transferrin. The normal saturation levels are 20-50%. When the saturation falls below 10%, it reveals that the patient has an absolute iron deficiency. With levels between 10-20%, it is more likely that the decrease is the result of an inflammatory state. And with iron overload, especially hereditary hemochromatosis, is usually associated with saturation that is well over 50%, often approaching 90-100%.
