Download RBC and WBC Disorders: Ch`s 9, 10, and 11 Chapter 11 RBC`s

RBC and WBC Disorders: Ch’s 9, 10, and 11
Chapter 11

RBC’s
o Function of the Red Blood Cells
 Transportation of oxygen to the tissues
 Hemoglobin binds some carbon dioxide (CO2) and carries it from the
tissues to the lungs
 The hemoglobin molecule is composed of two pairs of structurally
different polypeptide chains
o Each of the four polypeptide chains consists of a globin (protein)
portion of the heme unit, which surrounds an atom of iron that
binds oxygen
 Each molecule of hemoglobin can carry four molecules of oxygen
 The production of each type of globin chain is controlled by individual structural
genes with five different gene loci
 Mutations can occur anywhere in these five loci
o Erythropoiesis
 Red cells are produced in the red bone marrow after birth
 Until age 5 years, almost all bones produce red cells to meet growth needs;
after 5 years, bone marrow activity gradually declines
 After 20 years, red cell production takes place mainly in the membranous bones
of the vertebrae, sternum, ribs, and pelvis
 With this reduction in activity, the red bone marrow is replaced with fatty
yellow bone marrow
o Red Blood Cell Destruction
 The red blood cell has a life span of approximately 120 days
 It is broken down in the spleen
 The degradation products (iron and amino acids) are recycled
 The heme molecule is converted to bilirubin and transported to the liver
 It is removed and rendered water soluble for elimination in the bile
 Randoms
 Free, unconjugated (indirect) bilirubin is plasma insoluble before it gets
to the liver. It attaches to plasma proteins for transport to the liver,
where it is removed from the blood and becomes conjugated which
makes it water soluble.
 Conjugated (direct) bilirubin has joined with glucuronide which makes it
water soluble. It can then be excreted in the bile.
 When RBC destruction takes place in circulation it’s called hemolytic
anemia!
o


Lab Tests for RBC’s
 Red Blood Cell Count (RBC)
 Measures the total number of red blood cells in 1 mm3 of blood
 Percentage of reticulocytes (normally approximately 1% of our RBC count)
 Provides an index of the rate of red cell production
 Hemoglobin (grams per 100 mL of blood)
 Measures the hemoglobin content of the blood
 Hematocrit
 Measures the volume of red cell mass in 100 mL of plasma volume
Anemia
o Definition
 An abnormally low number of circulating red blood cells or level of hemoglobin,
or both
 Results in diminished oxygen-carrying capacity
o Causes
 Excessive loss (i.e. bleeding) or destruction of red blood cells (hemolytic anemia
is destruction of the RBC’s with the iron still being recycled)

o
Deficient red blood cell production because of a lack of nutritional elements or
bone marrow failure (say, your body isn’t making enough RBC’s to begin with.
They’re not being destroyed, you just don’t have as much as your body needs)
 *Remember* Anemia is not a disease, but an indication of some disease
process or alteration in body function.
Manifestations of Anemia
 Manifestations can be grouped into 3 categories! Also, the manifestations of
anemia depend on its severity, the rapidity of its development, and the affected
person’s age and health status
 Those resulting from tissue hypoxia due to decreased O2 delivery
 Those due to compensatory mechanisms
 The s/s associated with the pathologic process causing the anemia.
 The actual manifestations of anemia
 Impaired oxygen transport with the resulting compensatory
mechanisms
o Tachycardia happens because you don’t have enough O2 being
transported, so we’ll move what we do have around faster.
Sometimes the person can feel the palpitation of their heart.
 Reduction in red cell indices (numbers, basically) and hemoglobin levels
MCV, MCH, MCHC (describe cell size and hgb (hemoglobin)
concentration)
o MCV (mean corpuscular volume)- average size of the RBC’s
 MCV lows are Microcytic (smaller than normal) RBC’s
are seen in iron deficiency anemia, lead poisoning,
thalassemia
 MCV highs are macrocytic (larger than normal) are seen
in pernicious anemia and folic acid deficiency
 MCV is normal it’s called normalcytic (same size) is seen
in blood loss. You’re RBC’s aren’t fucked up, you just
don’t have enough of them
o MCH (mean corpuscular hemoglobin) measures the amount or
mass of hemoglobin present in one Red blood cell
 MCH low (hypochromic) and normal is normochromic
o MCHC (mean corpuscular hemoglobin concentration)- measures
the proportion of each RBC taken up with hemoglobin
 Signs and symptoms associated with the pathologic process that is
causing the anemia (pg 216)
o The decreased hemoglobin causes palor or paleness
o Tissue hypoxia because of no tissue transport
o The person feels weak or fatigued
o Dyspnea
o
o
o
o
Angina (chest pain)
Tachycardia happens because you don’t have enough o2 being
transported, so we’ll move what we do have around faster.
 Sometimes the person can feel the palpitation of their
heart because it’s going so fast
Classificaiton of Anemias (Table 33-2 from Brunner, p 1045)
 Hypoproliferative (you’re not making enough)
 Iron deficiency
 Folate and B12 ddeficiency
 Decreased EPO (erythropoietin)
 Cancer/Inflammation
 Bleeding
 GI, menorrhagia (excessive menstral bleeding), epistaxis (nose bleeds),
trauma. If it’s a slower bleed, sometimes you can lose up to 50% of your
blood before you start to get the S/S of it!
 Hemolytic (you’re body is making enough RBC’s, but they are being destroyed)
 Sickle cell, hypersplenism (enlargement of the spleen so it’s doing it’s
job too well of breaking down RBC’s), drug-induced, autoimmune
Hemolytic Anemias- Your blood cells are being prematurely destroyed, your body still
keeps the iron and other products of hemoglobin destruction, and an increase in
erythropoisis to compensate for the loss of red cells. The bone marrow is usually
hyperactive, resulting in an increase in the nbr of reticulocytes in the blood.
 Inherited disorders of the red cell membrane
 You inherit some shit from your parents that fucks up your RBC’s
 Hemoglobinopathies= your hemoglobin molecule is screwed up
 Sickle cell anemia (figure 11-8)- the cells are shaped like a sickle so they
don’t hold O2 as well as a normal RBC
o Figure 11-8= If the cell is full of oxygen it is normal shaped. Once
the oxygen leaves it, it kind of collapses to a sickle shape. If it’s
without oxygen in it for too long, it becomes irreversibly sickle
shaped. Once they are stuck like that, they stick to the vessel
walls easier, making your more likely for stroke and clots and all
that mess.
 Thalassemias- absent or defective alpha or beta chain of hemoglobin.
Occurs mostly in children
o Alpha- mostly Asians
o Beta- Mediterranean (greek and Italians mostly)
 Inherited enzyme defects
 About 10% people of African descent
 G6PD is the enzyme that is fucked up

Acquired hemolytic anemias
 Drugs, bacteria or other toxins, antibodies, and physical trauma cause
your RBC’s problems.
o
Anemias of Deficient Red Cell Production
 Iron deficiency anemia
 Megaloblastic anemias (super big, mega) Your RBC’s get way too fucking big
and don’t work properly.
 Cobalamin deficiency anemia (not enough B12)
o B12 comes from animal sources, so stupid vegans and whatnot
are usually the ones who get this, cause they don’t eat animals!
o Pernicious Anemia is a contributing factor to this. You lack an
intrinsic factor that helps do something to B12. When you don’t
have B12, the RBCs that are made are huge. I don’t know why,
they just are.
 Folic acid deficiency anemia
o Folic Acid comes from fresh, green, leafy vegetables
o Alcohol increases the amount of Folic acid you need
o Being preggers, especially in the beginning, you need lots more
folic acid
 Aplastic anemia
 You lose all of your blood cell making capacity
 Serious situation
 Chronic disease anemia
 Sometimes called anemia of chronic inflammation
o
Iron- Deficiency Anemia
 Etiology - Chronic blood loss
 Characterized by
 Low Hgb and Hct, decreased Fe (iron) and ferritin levels
 Dec # RBC, Microcytic, Hypochromic
 Irregular shape and size
 Manifestations
 Decreased O2 transport
o Fatigue, palpitations, dyspnea, angina, tachycardia
o Epithelial atrophy, waxy pallor, brittle nails
o smooth tongue, mouth sores in the corners of your mouth
o Dysphagia (difficulty swallowing), decreased acid secretion
o Pica – eating ice, dirt, starch…

o
o
o
Pica is the abnormal eating of these things! You don’t
have iron, so bitches go crazy and eat dirt to get iron!
Aplastic Anemia
 Bone marrow stem cells – reduction of RBCs, WBCs, platelets (the bone
marrow isn’t doing its freaking job)
 Etiology – Radiation, chemicals, toxins that suppress hematopoiesis,
Idiopathic
o Chloramphenical is an antibiotic that might be a cause of
aplastic anemia
 Manifestations of Aplastic Anemia
o Insidious or abrupt onset, at any age (insidious means
unnoticed)
o Weakness, fatigue, pallor, petechiae (those little red dots)
o Ecchymosis, bleeding from orifices (bruising)
 Treatment
o Stem cell replacement, bone marrow replacement. May treat
with blood transfusion while waiting to do the replacement
stuff.
Anemia of Chronic Disease
 Result of Chronic Infection, Inflammation, and cancer
 TB (tuberculosis), AIDS, RA (rheumatoid arthritis), SLE (systemic lupus
erythematosis), Hodgkin’s disease
 Pathogenisis
 Short, lifespan, decreased response of Epoietin (pg 223)
 Low, serum Fe (iron)
 Action of macrophages and lymphocytes in response to cell injury
o They think the short lifespan and low iron levels are because the
macrophages are sequestering iron in the spleen. So, they are
keeping the iron captive and not letting it function in your RBC’s
 Chronic Renal failure – normocytic, normochromic due to deficiency of Epoietin
 Uremic toxins and Nitrogen (these interfere with the actions of
Epoietin), hemolysis due to hemodialysis also contribute to the anemia
Red Blood Cell Components used in Transfusion Therapy
 Whole Blood
 Red Blood Cells
 Leukocyte-reduced blood cells
 Washed red blood cells
 Frozen red blood cells
o
o
Transfusion Therapy
 Provides the means for replacement of red blood cells and other blood
components
 Four major ABO blood types are determined by the presence of absence of two
red cell antigens: A and B
 The presence of D antigen determines the Rh-positive type
 The absence of the D antigen determines the Rh-negative type
S/S of a Transfusion Reaction
 Sensation of heat along the vein where the blood is being infused
 Flushing of the face
 Urticaria (rash or hive), headache, pain in the lumbar area
 Chills, fever, constricting pain in the chest
 Cramping pain in the abdomen
 Nausea, vomiting
 Tachycardia, hypotension, and dyspnea

Polycythemia
o Definition
 A condition in which the red blood cell mass is increased
o Types
 Relative polycythemia: results from a loss of vascular fluid and is corrected by
replacing the fluid
 Primary polycythemia: a proliferative disease of the bone marrow with an
absolute increase in total red blood cell mass accompanied by elevated white
cell and platelet counts
 Secondary polycythemia: results from increased erythropoietin levels caused by
hypoxic conditions such as chronic heart and lung disease

Diagnosis of Anemia in the elderly
o Complete physical examination
o Complete blood count
 Peripheral blood smear and a reticulocyte count and index
o Studies to rule out comorbid conditions such as malignancy, gastrointestinal conditions
that cause bleeding, and pernicious anemia