BLOOD TEST: clot etc.

BLOOD TESTS, CLOTTING AND DISORDERS:
http://people.eku.edu/ritchisong/301notes4.htm
Acidosis : below pH 7
alkalosis : above pH 7
Respiratory system and kidneys restore pH via negative feedback : ADH, Rennin and Angiotensisn
Homeostasis = hemostasis
Hemostasis= clotting
3 phases = vascular spasm -platelet plug - coagulation
Cascade Coagulation video : http://www.youtube.com/watch?v=co6ar6vVp70&feature=related
Hemostasis - prevention of blood loss from broken vessel (check this Hemostasis animation):
1 - Vascular spasm - vasoconstriction of injured vessel due to contraction of smooth muscle in the
wall of the vessel. This 'spasm' may reduce blood flow & blood loss but will not stop blood loss.
Serotonin causes the vascular spasm ex. Positive feedback (short term an dlocalized)
2 - Formation of a platelet plug - platelets aggregate at the point where a vessel ruptures. This
occurs because platelets are exposed to collagen (a protein found in the connective tissue located
just outside the blood vessel). Upon exposure to collagen, platelets release ADP (adenosine
diphosphate) & thromboxane. These substances cause the surfaces of nearby platelets to become
sticky and, as 'sticky' platelets accumulate, a 'plug' forms.
3 - Blood coagulation (clotting):
The result of all of this is a clot - formed primarily of fibrin threads (or polymers), but also
including blood cells & platelets.
Blood clots in the right places prevent the loss of blood from ruptured vessels, but in the wrong
place can cause problems such as a stroke (see below under inappropriate clotting).
Clot retraction:
•
•
"tightening" of clot
contraction of platelets trapped within clot shrinks fibrin meshwork, pulling edges of
damaged vessel closer together
Over time (with the amount of time depending on the amount of damage), the clot is dissolved and
replaced with normal tissue.
Fibrinolysis:
•
•
dissolution of clot
mechanism = plasminogen (a plasma protein) is activated by many factors & becomes
PLASMIN. Plasmin then breaks down fibrin meshwork & phagocytic WBCs remove
products of clot dissolution
Blue arrows = stimulation; red arrows = inhibition. tPA is released by damaged endothelium
(Source: en.wikipedia.org/wiki/Fibrinolysis)
Blood clotting SUMMARY
Serotonin = vascular spasm + tissue thromboplastin + prothrombin/Ca++ =thrombin + fibrinogen =
fibrin = clot
Disorders of hemostasis or Inappropriate clotting:
thrombus - clot formed in an intact vessel, possibly due to:
o
roughened vessel walls (atherosclerosis; see normal & occluded coronary arteries
below)
o
o
slow-moving blood (e.g., in varicose veins) = small quantities of fibrin form &
accumulate
check this animation about deep vein thrombosis
embolus - 'moving' clot
•
Source: http://www.ors.od.nih.gov/medart/portfolio/Donny/embolus.html
•
Thrombus and embolus : video: http://people.eku.edu/ritchisong/301notes4.htm
Clotting: normal is 2-6 min decreases with Ca dropping and aspirin increasing
Anticoagulants such as HEPARIN which is made by mast cells and basophils inhibits
prothrombin from converting into thrombin
Warafrin: Vit K antagonist so 4 CF cannot be made
Excessive bleeding:
•
•
Hemophilia
o genetic 'defect'
o inability to produce certain clotting factor(s)
Thrombocytopenia
o abnormally low platelet count
o most persons have idiopathic thrombocytopenia (= unknown cause) while in others it's
an autoimmune disease
Thrombocytopenia is a condition where platelet counts are lower than normal, potentially leading
to mild to serious bleeding. This bleeding can happen inside the body (internal bleeding) or on the
skin. A normal platelet count is 150,000 to 450,000 platelets per microliter of blood. A count of
less than 150,000 platelets per microliter is lower than normal, but the risk for serious bleeding
doesn't occur until the count becomes very low—less than 10,000 or 20,000 platelets per microliter.
Milder bleeding sometimes occurs when the count is less than 50,000 platelets per microliter.
Several factors can cause a low platelet count, such as:
•
The bone marrow doesn't make enough platelets.
•
•
•
The bone marrow makes enough platelets, but the body destroys them (autoimmunity) or
uses them up.
The spleen holds onto too many platelets. The spleen is an organ that normally stores about
one-third of the body's platelets. It also helps your body fight infection and remove unwanted
cell material.
A combination of the above factors.
How long thrombocytopenia lasts depends on its cause. It can range from days to years. The
treatment for this condition also depends on its cause and severity. Mild thrombocytopenia most
often doesn't need treatment. If the condition is causing serious bleeding, or if you're at risk for
serious bleeding, you may need medicines or blood or platelet transfusions. Rarely, the spleen may
need to be removed. Thrombocytopenia can be fatal, especially if the bleeding is severe or occurs
in the brain. However, the overall outlook is good, especially if the cause of the low platelet count
is found and treated (Source: NHLBI).
Blood tests: know how to perform these, read then and interpret
Blood typing
Talliquist: preliminary quantitative % Hb. Used as an indicator for anemia
Erythrocyte Sedimentation rate:
http://medical-dictionary.thefreedictionary.com/Blood+sedimentation
Definition
The erythrocyte sedimentation rate (ESR), or sedimentation rate (sed rate), is a measure of the settling of red blood cells in a tube of
blood during one hour. The rate is an indication of inflammation and increases in many diseases.
Lower rate : RBC abnormalities such as sickle cell
Higher Rate: Menses, pregnant, anemic
Very high rate; infection or condition of tissue destruction, cancer, rheumatoid arthritis
Normal results
A normal value does not rule out disease. Normal values for the Westergren method are: Men 0 mm/hour-15
mm/hour; women 0 mm/hour-20 mm/hour; and children 0 mm/hour-10 mm/hour.
Abnormal results
The highest ESR levels are usually seen in a cancer of a certain type of white blood cell (multiple myeloma) and
rheumatoid disease, such as rheumatoid arthritis. Many other diseases also increase the ESR: infection, kidney
disease, anemia, diseases involving white blood cells, cancer, and autoimmune and inflammatory diseases.
Any disease that changes the shape and size of red blood cells decreases the ESR. Distorted cells, such as with
sickle cell disease, do not stack, and consequently do not settle far, even in the presence of an ESR-associated
disease. Diseases that cause the body to make less protein or extra red blood cells also decrease the ESR.
Hemarocrit: % of RBC per unit volume
Too high = polycythemia
- bone marrow cancer
- slide: immature,
nucleated RBC
o
Anemia:
http://www.unm.edu/~mpachman/Blood/a
nemias.htm
How to diagnose?
http://www.youtube.com/watch?v=pGTu2a
DbLpg
Anemia from RBC loss:
http://www.youtube.com/watch?v=1ueLaBS9_dM&feature=channel
Types of Anemias
a. decrease in RBC number
b. inadequate Hb in RBC
c. Abnormal Hb in RBC
Liver and jaundice: due to a buildup of bilirubin
Macrophage phagocytizes RBC in spleen, liver and bone marrow.
1. heme is separated from globin
2. Fe is removed from heme by transferrin
3. Biliverdin is green inside the macrophage and converted into bilirubin in the blood
4. Bilirubin in the blood goes to liver
5. Liver secretes bilirubin into bile
6. Bile goes to LI where bacteria convert bile into urobilinogen
a. Goes back to blood as urobilin (yellow pigment) and is reoved by kidneys
b. sterobilin (brown pigment feces)
Ex. Neonatal due to immature liver, blue wavelengths of light breaks it up
Ex. Hepatitis: liver infected
Ex. Alcohol: liver destruction
Cord Blood: http://www.youtube.com/user/cordbloodregistry?v=96DItviGvKI