blood after breakdown Flashcards
What role do plasma proteins play in maintaining plasma volume?
Plasma proteins create osmotic pressure, which helps to maintain plasma volume and draw leaked fluid back into circulation.
What happens if there is a decrease in plasma proteins?
A decrease in plasma proteins results in a reduced plasma volume, as less osmotic pressure is available to draw fluid back into circulation.
What is Hematopoiesis and where does it occur in adults?
Hematopoiesis (Blood Cell Formation) occurs in red bone marrow (myeloid tissue).
Found primarily in the axial skeleton, pectoral and pelvic girdles, and proximal epiphyses of the humerus and femur in adults.
Blood cells are produced in varying numbers in response to the body’s needs and stimuli.
On average, the red marrow produces 1 ounce of new blood containing 100 billion cells every day.
After maturation, cells are discharged into surrounding blood vessels.
What is the hemocytoblast and how does it contribute to blood cell formation?
Hemocytoblast (blood cell former) is a common stem cell in red bone marrow.
It gives rise to two types of stem cells:
Lymphoid stem cell: Produces lymphocytes.
Myeloid stem cell: Produces all other types of formed elements (e.g., red blood cells, platelets, and other white blood cells).
Once a cell is committed to a specific blood pathway, it cannot change.
What happens to red blood cells (RBCs) as they age, and how are their components recycled?
RBCs are anucleate, meaning they cannot synthesize proteins, grow, or divide.
As RBCs age (100-120 days), they become rigid and break apart.
Their remains are eliminated by phagocytes in the spleen, liver, and other tissues.
Recycling process:
Iron is stored as ferritin for reuse.
The heme group is broken down to bilirubin, secreted into the intestine, and converted into stercobilin, which is excreted in feces.
Globin is broken down into amino acids, which are released into the bloodstream.
How are red blood cells (RBCs) formed, and what is the process from hemocytoblast to mature RBC?
Lost blood cells are replaced more or less continuously by the division of hemocytoblasts in the red bone marrow. The developing RBCs divide many times and then begin synthesizing huge amounts of hemoglobin. When enough hemoglobin has been accumulated, the nucleus and most organelles are ejected, and the cell collapses inward. The result is the young RBC, called a reticulocyte (rĕ-tik′u-lo-sīt) because it still contains some rough endoplasmic reticulum (ER). The reticulocytes enter the bloodstream to begin their task of transporting oxygen. Within 2 days of release, they have ejected the remaining ER and have become fully functioning erythrocytes. The entire developmental process from hemocytoblast to mature RBC takes 3 to 5 days.
The rate of erythrocyte production is controlled by a hormone called
erythropoietin (ĕ-rith″ro-po-e′tin). Normally a small amount of erythropoietin circulates in the blood at all times, and red blood cells are formed at a fairly constant rate. Although the liver produces some, the kidneys play the major role in producing this hormone. When the blood level of oxygen begins to decline for any reason, the kidneys (a convenient location to monitor blood) step up their release of erythropoietin. Erythropoietin targets the bone marrow, prodding it into “high gear” to turn out more RBCs. (Follow this sequence of events in Figure 10.4.)
How is red blood cell (RBC) production regulated?
RBC production is primarily controlled by the body’s need for oxygen, not the relative number of RBCs in the blood.
An overabundance of RBCs or excess oxygen in the bloodstream decreases erythropoietin release, which slows RBC production.
Erythropoietin is a hormone that stimulates RBC production, and its release is triggered when the body’s oxygen demands are not being met.
How are leukocytes and platelets produced and regulated?
Leukocyte (white blood cell) production is stimulated by colony stimulating factors (CSFs) and interleukins, which prompt red bone marrow to produce leukocytes and enhance their ability to protect the body.
These factors are released in response to inflammatory signals, certain bacteria, or their toxins.
Platelet production is accelerated by the hormone thrombopoietin, which is produced by the liver and stimulates megakaryocytes to produce platelets, though the exact regulation process is not fully understood.
What is a bone marrow biopsy, and when is it performed?
A bone marrow biopsy is a procedure in which a special needle is used to withdraw a small sample of red bone marrow from flat bones like the ilium or sternum.
This biopsy is performed when bone marrow problems or conditions such as leukemia are suspected.
The sample is then examined microscopically to assess the condition of the marrow and the presence of any abnormal cells.
What is hemostasis, and how is it triggered?
Hemostasis is the process of stopping bleeding when a blood vessel wall breaks.
It involves a fast and localized response that includes reactions by substances present in plasma and those released by platelets and injured tissue cells.
Normally, blood flows smoothly, but when a vessel is damaged, hemostasis is initiated to prevent excessive blood loss.
What are the three major phases of hemostasis?
Hemostasis involves three major phases, which occur in rapid sequence: vascular spasms, platelet plug formation, and coagulation, or blood clotting. Blood loss at the site is prevented when fibrous tissue grows into the clot and seals the hole in the blood vessel.
Hemostasis occurs as follows (Figure 10.5):
Vascular spasms occur. The immediate response to blood vessel injury is vasoconstriction, which causes blood vessel spasms. The spasms narrow the blood vessel, decreasing blood loss until clotting can occur. (Other factors causing vessel spasms include direct injury to the smooth muscle cells, stimulation of local pain receptors, and release of serotonin by anchored platelets.)
Platelet plug forms. Platelets are repelled by an intact endothelium, but when the underlying collagen fibers of a broken vessel are exposed, the platelets become “sticky” and cling to the damaged site. Anchored platelets release chemicals that enhance the vascular spasms and attract more platelets to the site. As more and more platelets pile up, a platelet plug forms.
Coagulation events occur. At the same time, the injured tissues are releasing tissue factor (TF), which interacts with PF3 (platelet factor 3), a phospholipid that coats the surfaces of the platelets. This combination interacts with other clotting factors and calcium ions (Ca2+), which are essential for many steps in the clotting process, to form an activator that leads to the formation of thrombin, an enzyme. Thrombin then joins soluble fibrinogen (fibrin′o-jen) proteins into long, hairlike molecules of insoluble fibrin. Fibrin forms a meshwork that traps RBCs and forms the basis of the clot (Figure 10.6). Within the hour, the clot begins to retract, squeezing serum (plasma minus the clotting proteins) from the mass and pulling the ruptured edges of the blood vessel closer together.
when the clot finishes
Normally, blood clots within 3 to 6 minutes. As a rule, once the clotting cascade has started, the triggering factors are rapidly inactivated to prevent widespread clotting. Eventually, the endothelium regenerates, and the clot is broken down. Once these events of the clotting cascade were understood, it became clear that placing sterile gauze over a cut or applying pressure to a wound would speed up the clotting process. The gauze provides a rough surface to which the platelets can adhere, and the pressure fractures cells, increasing the release of tissue factor locally.
Major Disorders of Hemostasis
Undesirable Clotting:
Thrombus: A clot that forms in an unbroken blood vessel. It can obstruct blood flow and lead to tissue damage.
Example: Pulmonary thrombosis can block blood flow to the lungs, leading to death of lung tissue and hypoxia (low oxygen levels).
Embolus: A clot that breaks off and floats in the bloodstream. It can travel and lodge in smaller blood vessels, causing issues like:
Cerebral embolus: Can cause a stroke by blocking blood flow to the brain.
Causes of Undesirable Clotting:
Damage to blood vessel walls (e.g., burns, physical blows, fatty material accumulation).
Slow blood flow or blood pooling, especially in immobilized patients, where clotting factors accumulate.
Anticoagulants: Used to prevent clot formation in thrombus-prone patients. Common examples include:
Aspirin
Heparin
Warfarin
Bleeding Disorders:
Thrombocytopenia: Low platelet count, leading to excessive bleeding. Causes include:
Bone marrow suppression (e.g., cancer, radiation, certain drugs).
Spontaneous bleeding from small blood vessels.
Petechiae: Small purple blotches resembling a rash.
Clotting Factor Deficiency: Insufficient clotting factors can result from liver dysfunction or genetic conditions.
Vitamin K deficiency can be treated with supplements.
Severe liver impairment (e.g., cirrhosis, hepatitis) may require whole blood transfusions.
Hemophilia: Hereditary bleeding disorder due to the lack of clotting factors. Causes prolonged bleeding from minor trauma and joint damage.
Treatment: Plasma transfusions or injections of purified clotting factors.
Risks: Hemophiliacs have historically been at risk for blood-transmitted diseases (e.g., hepatitis, HIV), though genetic clotting factors and vaccines have reduced this.
