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 slow-moving blood (e.g., in varicose veins) = small quantities of fibrin form & accumulate

o 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/anemias.htm How to diagnose? http://www.youtube.com/watch?v=pGTu2aDbLpg 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