Disorders of the Blood
This attempts to summarize the handout for the upcoming test. There is a lot of
information in this file, and I believe it all to be important, or at least testable. One
omission I made is treatment. Lots of space could have been wasted on specific drugs or
experimental procedures to medically address the conditions discussed. If these things
are important to you, you will need to look them up. This document is very dense
reading, and it does come late, but hopefully not too late to help.
Background
Bone marrow
Site of formation of most of blood’s cellular elements
RBC, platelets, many WBC (neutrophils)
Lymphocytes are formed in lymph tissue
Monocytes are formed in the reticuloendothelial system
RBCs
Need protein, Fe, Co, Cu, Mg, B12, C, folic acid, erythropoietin, ACTH to form
properly
RBC last 120 days, number 25 trillion
Reticulocytes – in packet
Are source of bilirubin/urobilinogen (RBC>Hemoglobin>porphyrin
ring>bilirubin>liver>bilirubin digluceronide>GI>urobilinogen>urine/feces)
Erythropoietin is produced by kidneys. Extra is produced in anoxic or hypoxic
states
Fe metabolism
Body’s iron is in hemoglobin (2/3), stores (1/5), myoglobin/enzymatic (rest)
Transport iron is bound to transferring
WBC
Neutrophils
Aka neutrophilic myelocytes/granulocytes, polymorphonuclear leukocytes
Formed only in bone marrow, from myeloblasts (thus the aka)
Cause increase: exercise, eat, infection, B12 increase, neoplasm,
polycythemia vera
Cause decrease: viral infection, gold/heavy metal toxin, radiation
Eisonophils
Aka eosinophilic granulocytes/myelocytes
Function to phagocytize immune complexes (I remember MEN are fags –
Monocytes/Eosinophils/Neutrophils)
Respond in allergic reactions, Hodgkins disease, parasitic infection,
allergic dermatitis, bronchial asthma, allergic rhinitis
Sometimes a measure of adrenal cortical activity
Basophils
Aka basophilic granulocytes/myelocytes
Unknown function, in other classes, mast cells have been called “fixed
basophils”
Release histamine, as do mast cells
Lymphocytes
Come from lymphatic tissue, not bone marrow (are not myeloid)
Increased in infectious mononucleosis, lymphocytic leukemia
Any increase in the lymphocytes will result in a relative ‘penia (lack) of
another blood element
Monocytes
Origin in the reticuloendothelial system, not bone marrow
Platelets
Origin in bone marrow, from megakaryocytes
Their number seems to be regulated by the spleen (no spleen, higher #)
Have a life span of 11 days (not in handout chart)
Hematocrit
Heparin is the anticoagulant used (lavender top)
Hemoglobin
Measured by size of the band of unstained area, or by spectrophotometer
RBC count
See Dr. B’s notes
Blood indices
See Dr. B’s notes
MCV – volume. Tells if the cell is macrocytic/microcytic/normocytic
MCH – weight of Hb. Tells if the cell is hyperchromic/hypochromic…
MCHC – how much of each RBC is Hb
Color index – another value for MCH (>1 is hyperchromic…)
WBC count
Polymorphs (segmented neutrophils) are the majority
Generally, when the myeloid-origin parts of blood are in excess, that is called
leukocytosis, and when they are depressed, that is called leukopenia
Blood smear
Differential blood count
May tell if there is an abnormal number of one type of cell (eosinophilia),
or if there are abnormal cells (leukemia)
Abnormalities of red cells
Large RBC – macrocytosis or reticulocytosis
Stippled (dotted) RBC – lead poisoning, reticulocytosis
Target cells – Mediterranean anemia, hypertonicity
Reticulocyte count
Normal is 0.5 to 1.5%
See Dr. B’s notes
Serum bilirubin
Since bilirubin comes from dead Hb, to measure it is to estimate the destruction of
RBCs
Normally less than 1.0 mg per cent
Gastric analysis
Absence of B12 – pernicious anemia
Absence of stomach HCl – pernicious anemia
Occult blood in the stools
Positive guaiac test
Bone marrow aspiration
Basically, a biopsy taken of the bone marrow of flat bones (sternum)
The Anemias
The 2 page outline says that anemia can be caused by 3 things: 1. loss of blood. 2. low
blood production. 3. high blood destruction
Anemias due to blood loss
Acute hemorrhage causes blood loss. Even so, blood counts are normal for
several hours following hemorrhage due to vasoconstriction, hemoconcentration
Chronic hemorrhage such as peptic ulcer may be more difficult to find
A sequella of chronic blood loss is iron deficiency, and that particular anemia
(hypochromic, microcytic)
Anemias due to decreased production of blood
Iron deficiency anemia
Menstruation, pregnancy may reduce stores of Fe in women
Also increased Fe need in fever, hyperthyroid conditions
Spoon-shaped fingernails
Numb or tingly fingers
Hypochromic, microcytic means color index below 1, & low MCV/MCH
Anisocytosis and poikilocytosis
Often confused with hemolytic anemia with spherocytosis (but that
condition will have increased bilirubin/urobilinogen, overactive bone
marrow)
Macrocytic/megaloblastic anemias (B12, folic acid deficiencies)
Pernicious anemia
Is related to B12, HCl deficiencies
3 categories of symptoms
1. weak, pallor, fatigue, dyspnea, ankle edema
2. GI changes: appetite loss, sore tongue, nausea
3. CNS: dorsolateral columns, dizzy, numb, tingle,
parasthesia, staggering gait, poor reflexes, +
Romberg’s, loss of bladder control
Hyperchromic, anisocytosis, poikilocytosis, macrocytosis
Lab determination
Absent gastric HCl, Leukopenia, antibodies to gastric
mucosa (autoimmune?), B12, Folate levels
Anemias due to depressed bone marrow activity (low blood production)
Bone marrow malfunctions due to toxins, drugs
WBC, RBC, platelets are all depressed (at least the WBC produced in the bone
marrow by myeloid tissue)
Normochromic
Relative lymphocytosis (reduced myeloid WBCs)
Marrow biopsy yields few WBC
Treated by transfusion of marrow
Hypersplenism
Excess destruction of blood elements formed in the bone marrow
Suspected when other signs of anemia present with splenomegaly
Hemolytic anemias (anemias due to high blood cell destruction)
Normocytic, bilirubinemia, urobilinogenemia/urea, reticulocytosis (once again,
remember that bilirubin and urobilinogen come from the hemoglobin freed in the
destruction of the RBC)
Sickle cell anemia “S”
Negroes
Fever, muscle and joint pain, leg ulcers, thrombus formation
Treated by transfusion, treating symptoms
Mediterranean anemia “F”
Aka leptocytosis, thalassemia
Fetal hemoglobin persists to adulthood
Bone pain, x ray changes(hair on end) are diagnostic
Primaquine sensitivity
Enzyme deficiency (glucose-6-phosphate dehydrogenase)
Heridetary spherocytosis
Small diameter, deeply stained (microcytic, hyperchromic)
These cells are mechanically very fragile
Summary
In analyzing an anemia, determine first if there is blood loss. Then, examine stool
for occult blood loss. Jaundice or other manifestation of bilirubin/urobilinogen would
indicate a hemolytic anemia. Pernicious anemia is characterized by CNS symptoms and
smooth tongue. Lymphoma may be indicated by splenomegaly, hepatomegaly,
lymphadenopathy. Also look at blood indexes, and know the numbers. Dr. B. may not
state that a cell is hyperchromic. He may just list a value, and from that, you would have
to judge what the anemia is. I have listed all the macro/micro/hyper descriptions in bold
type. Normochromic anemia presents with bone marrow deficiency problems.
Hypersplenism is associated with leukopenia, anemia, and thrombocytopenia, as it is
involved in destruction of tissue of myeloid origin. Leukopenia, thrombocytopenia, and
anemia may also be related to aplastic anemia.
The Leukemias
Polycythemia vera (erythrema)
High Hb
Few symptoms unless there are complications (prutitis-itching, plethora-reddish
cyanosis, venous engorgement, and splenomegaly)
Also presents with leukocytosis, thrombocytosis, reticulocytosis, elevated
hematocrit, increased blood volume and increased viscosity, low sedimentation
rate, hypercellular bone marrow. It seems that whatever causes the increased
RBC production also stimulates the bone marrow to “be all it can be”
Thrombosis is common (cerebral, mesenteric, and coronary vessels)
Heart is strained leading to CHF
Treated by reduction in bone marrow activity (radiation, TEM drugs)
There is a section of lab findings (actual numbers you would get as test results).
Basically, there would be:
high RBC, WBC, Hematocrit, Hb, platelets, reticulocytes, total blood
volume, red cell volume, plasma volume, basal metabolic rate
low sed rate
Secondary erythrocytosis
Causes: hypoxemia (COPD, pulmonary arteriosclerosis, CV shunt, high altitude
conditions), overstimulation of bone marrow (stress, Cushing’s syndrome, tumor
causing excess erythropoietin, Co poisoning)
Other signs and symptoms of the above conditions will give away the true cause
of the disorder.
The leukemias
Many immature WBC in peripheral blood and marrow
When neutrophils are the problem, are called myeloid leukemias
When lymphocytes are involved, are called lymphocytic leukemias
Aleukemic leukemia
Characterized by normal or low WBCs
Leukocyte alkaline phosphatase
Present in granulocytes. When absent, think of granulocytic (myelocytic)
leukemia
Thymus gland may be source of Hodgkins disease, multiple myeloma
Myelogenous leukemia
When acute, tends to affect children. Due to overproduction of
myelocytes, the production of thrombocytes by the bone marrow is
reduced. This can lead to bleeding, and therefore anemia.
When chronic, tends to affect adults. Often see splenomegaly (remember
hypersplenism? This is different.)
There is hyperplasia (excess cell production) of myeloid cells, and relative
lack of RBC and megakaryocyte (platelet) production
Lymphatic (lymphocytic) leukemia
When acute or subacute, tends to affect children. Lymphatic centers
(nodes) throughout the body are enlarged. Lymphocytes may get in and
damage the function of any organ system in the body, and they commonly
affect bone marrow. When they do this, thrombocyte production is
reduced, and excess bleeding may occur.
When chronic, tends to affect adults late in life. Often, a pt may live with
this condition symptom free. However, signs may include
hepatosplenomegaly, lymphadenopathy
Leukemoid reactions
“Leukemia-like” conditions
Complete recovery is common
May be induced by drugs, TB, others
Erythroleukemia
Aka di Guglielmo’s Syndrome
This is an acute leukemia, with immature RBC precursors
Erythroblasts have abnormal forms, function
Presents with anemia
RBCs are nucleated
Myeloid metaplasia
Centers of hemopoieses (blood cell formation) form outside bone marrow
(liver, spleen, others)
Hepatosplenomegaly and leukocytosis both occur
Death in 2 to 5 years
Infectious mononucleosis
This is a leukemoid reaction, of viral origin (Epstein-Barr Virus)
Seen in children and young adults
One survived attack gives immunity
First symptom is sore throat, low fever, lymphadenopathy, splenomegaly,
leukocytosis
Heterophile antibody test
Multiple myeloma
Diagnosed by study of bone marrow
More common in adult males over 50
Begins as a plasma cell tumor and metastasizes to bone
Symptom is bone pain
Shows on x ray as a punched out lesion in skull and flat bones
Shows an electrophoresis peak in the gamma globulin range
Bence Jones protein is present
Waldenstrom’s macroglobulinemia
Problem with the reticuloendothelial system
Lymphocytoid cells (whatever those are) make large globulins
Symptoms are weight loss, susceptibility to infection (assuming, I
suppose, that the globulins produced are nonfunctional), retinal
hemorrhage, purpura, hepatosplenomegaly, heart failure
Also shows Bence Jones protein
Hodgkin’s disease
Disease of lymphatic origin
Lymph nodes enlarge, but painlessly
Other symptoms may occur due to compression of local organs
Stages 1. Disease in 1 node
2. Disease in 2 nodes, both above or both below the diaphragm
3. Disease on both sides of the diaphragm
4. Disease on both sides of diaphragm, but not confined to spleen
or nodes
Lymphosarcoma
Malignant disease originating in the lymphatic system
Results in death
Lymphadenopathy may locally compress and affect tissue