Hematology Flashcards
3 parts of blood
Plasma: 55%, least dense
Buffy coat: <1% leukocytes& platelets
Erythrocytes: 45%, most dense
3 functions of blood + sub functions
Transport: O2, CO2, wastes, hormones
Regulation: body temp, pH, blood volume
Protection: Clotting, immune system
Characteristics of blood
Temp: 38 degrees C
pH: 7.35-7.45
Volume: 5-6 l (8% of body weight in kg)
Components of plasma
90% water ions (electrolytes) organic molecules trace elements & vitamins gases (O2, CO2 not in RBC)
Organic molecules in plasma
amino acids proteins: albumin, globulin, fibirinogen glucose lipids nitrogenous waste (uric acid, urea)
most common protein & where it’s made
albumin, liver
formed elements
erythrocytes, leukocytes, platelets
how many RBCs male/female
4.5 million/microliter (F), 5.5 mill (M)
What is Hematocrit & ranges for M/F
amount of RBCs per test tube volume. 42% (F), 47-48% (M)
shape & size of RBCs
biconcave, round, like donut w/o hole all the way through. 7.5 micrometer
hemoglobin, location and structure
RBCs are big bags full of haemoglobin molecules. haemoglobin binds O2 and is made up of 4 protein chains (globins, one alpha, one beta) and one heme which binds to iron with 2+ charge
what does oximeter measure
amount of O2 bound to haemoglobin
oxy vs deoxy hemoglobin
haemoglobin bound to 4 o2 is oxyhemoglobin. less than 4 is deoxyhemoglobin
how many haemoglobin fits into 1 micrometer
250 million
hematopoiesis
production of blood
production of RBCs is called
erythropoiesis
where do all formed blood elements derive from
hematopoietic stem cell/hemocytoblast
pathway of development for erythrocyte
stem cell
committed cell: proerythroblast
reticulocyte (baby RBC)
process involves committing to becoming RBC, filling up with haemoglobin, and kicking out organelles and nucleus.
hormone that regulates RBC production, where does it come from and what stimulates it’s activity
erythropoietin, kidneys, testosterone
dietary influences on RBC production
iron, B12 & folic acid, intrinsic factors
Iron storage and transport
iron is toxic in its free form. it has to be stored and transported within a storage/transport protein. Iron is mainly stored in the liver
iron storage proteins
ferritin and hemosiderin
iron transport protein
transferrin
B12 and folic acid role in RBC production
important for appropriate DNA replication
intrinsic factor role and what happens without it
lives in lining of stomach and allows absorption of B12 in GI tract. lack of intrinsic factor can lead to pernicious anaemia
how long do RBCs live
120 days
spleen role in destruction of RBCs
“cemetery” of RBCs, old ones get stuck in the narrow capillaries of the spleen where they are broken down by macrophages
what is recycled when RBCs are destroyed
iron and storage proteins, globins (proteins) are broken into amino acids and reused
bilirubin
pigment that comes from the breakdown of heme. called chief bile pigment, it makes bile green. it’s secreted into the intestine where it becomes stercobilin, which makes feces brown. liver failure pts sometimes have green or gray feces.
polycythemia
too many RBCs
anemia
too few RBCs/some component is missing
hemorrhagic anemia
loss of blood from bleeding
hemolytic anemia
something is destroying RBCs
aplastic anemia
destroys red marrow
nutritional anemia
not eating well
thalasemia
missing a globin–genetic. common in ashkenazi jews
sickle cell anemia
a substituted amino acid changes the shape of haemoglobin causing RBCs to get stuck in capillaries
number of WBCs in blood
much fewer than RBCs
4,800-10,800mm3
primary function on WBCs
fight infections
differences of WBC from RBC
i. Number of cells present in blood
ii. Diapedesis: WBC has the ability to exit out of the blood vessels to get to the tissue
iii. Ameboid action: WBCs ability to move and go where they need to go
5 types of WBCs
granulocytes: neutrophils, eosinophils, basophils,
agranulocytes: lymphocytes, monocytes
(never eat bananas, let monkeys)
in order of abundance: never let monkeys eat bananas
granulocytes vs agranulocytes
d. Granulocytes: contain lots of little “rocks”, which contain chemicals
neutrophils: primary function, nucleus shape
can undergo phagocytosis. Primarily seen in presence of bacterial infection
Multilobed/segmented nucleus. Polymorpho nuclear cells (PMNs). If neutrophil has banded nucleus instead of segmented, it’s an immature neutrophil. This is referred to as “left shift”.
eosinophils: function, nucleus shape
known to fight worms and allergic reactions and weird diseases. Bilobal nucleus
basophils: function, nucleus shape
work the same way as mast cells. Filled with histamine which trigger an inflammatory reaction. Nucleus shaped like a swan or S.
lymphocytes function & where they hang out, structure, 2 types
- Hang out in lymphatic tissue (spleen, nodes)
- Tiny cell, mostly made up of its nucleus
- 2 types: B lymphocytes and T lymphocytes
monocytes function, nucleus shape, size
- Largest of all WBC
- U-shaped nucleus
- Macrophage (eat a lot)
- Viruses, Tb, parasites
production of WBCs is called
leukopoiesis
chemical that drives leukopoiesis
interlukins
Colony stimulating factors
Each type of WBC has a stimulating factor, so that production can be tailored to what infections are present.
leukocytosis
too many WBCs
leukopenia
too few WBCs
platelets aka
thrombocytes
what are platelets
Fragments of cells filled with chemicals that help stop bleeding through clotting
where do platelets derive from
Comes from a type of cell called megakaryocytes, which comes from hematopoietic stem cells just like RBCs and WBCs
how many platelets in microliter of blood
150,000-300,000
thrombocytopenia
too few platelets
thrombocytosis
too many platelets
meaning of hemostasis and 3 steps
stop bleeding.
vascular spasm, platelet plug formation, coagulation
vascular spasm
decrease in the diameter of the blood vessel (vasoconstriction) so that less blood can leak out.
a. Usually seen in smaller blood vessels b/c larger vessels cannot decrease in size due to importance of circulation
b. Spasm response increased with increased damage
activation of platelets
activated by chemicals or interaction with other platelets. Inactive platelets are smooth, when activated they get spiky and release their contents
chemicals released from platelets and what they do
i. Seratonin: increases vascular spasm
ii. ADP: causes aggregation (platelets coming together)
iii. Thromboxane A2: increases both of above
Von Willebrand factor
protein in the plasma. When platelets become activated this protein helps them stick together.
prostaglandin
released by endothelial cells lining the blood vessels. Inhibitory for the formation of platelets
how many clotting factors (coagulants are there)
13, Designated by roman numerals. In the order they were discovered, not sequence they’re used
intrinsic pathway
activated by trauma inside the blood vessel. slow process because many steps
extrinsic pathway
requires tissue trauma to occur. fast process because it has fewer steps
common pathway
intrinsic and extrinsic pathways leads to common pathway. Common pathway begins with factor 10. Factor 10 activates prothrombin activator, this takes prothrombin to thrombin. Thrombin makes fibrinogen which makes fibrin. Fibrin is the clot, which is tied together by factor 13.
fibrinolysis & plasminogen
a. Fibrinolysis: the process of breaking down fibrin (the clot) as a part of healing
i. Plasminogen is wrapped up inside the clot and is an inactive bomb. Endothelial cells in vessels release tissue plasminogen activator (TPA) which activates plasmin, breaking down the fibrin mesh of the clot
intrinsic ways to inhibit clot formation
large vessels inhibit clots due to velocity
Antithrombin III: protein that inactivates thrombin so clotting rcess can’t be initiated.
medications that inhibit clot formation and examples
fibrinolytics
heparin: increases activity of antithrombin III
aspirin
coumadin
thromboembolytic
too many clots
Disseminated intravascular coagulopathy
Causes clotting that uses up too many clotting factors which causes bleeding.
thrombocytopenia
too few platelets, can be caused by impaired liver function and not enough vitamin K
hemophilia + 3 types
missing particular clotting factors
- A—classic—missing factor VIII
- B—factor IX
- C—Factor XI—not genetic
blood classifications
- A 42%
- B 10%
- AB 3%
- O 45%
antigens
substance that causes generation of antibodies
antibodies
attack and neutralize antigens and are specific to an antigen
universal recipient
type AB
universal donor
type O
Rh factor
- D antigen (+), 85% of population
2. Without antigen you are Rh -
- Erythroblastosis fetalis / hemolytic disease of the newborn
a. If someone who is Rh negative gets pregnant with an Rh+ baby, they start developing Rh antibodies
b. If they get pregnant a second time with an Rh+ baby, these antibodies start attacking the antigens on the RBCs of the baby
c. Drug called Rhogam which prevents the formation of Rh antibodies.
d. If pregnant person has received a blood transfusion with Rh antibodies in the past it may also affect the first baby.
e. This is the reason O- is most often given in transfusions
4 types of leukaemia
Acute/chronic myelocytic
Acute/chronic lymphocytic
Developmental paths of different types of leukemia
Chronic comes from fully developed leukocytes; myelocytic from granular and lymphocytic from agranular
Acute comes from promyelocyte or lymphocyte precursor cells (earlier in developmental pathway)
