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Platelets ✔Correct Answer-Derived from megakaryocytes in the bone marrow
1/3 are stored in the spleen and released when needed
All but which of the following is not true about platelets
A. Erythropoietin stimulated production
B. Made from megakaryocytes
C. Originate in bone marrow
D. Stored in spleen ✔Correct Answer-A. Erythropoietin stimulated production is false.
Platelets production occurs via thrombopoietin
Role of the endothelium ✔Correct Answer-Prevents platelets and plasma coagulation factors from
interacting with the underlying thrombogenic subendothelial ECM
What do health intact endothelial cells produce ✔Correct Answer-PGI2
NO
ADPase
TPA
What does the endothelium prevent ✔Correct Answer-platelet adhesion and aggregation
Stages of hemostasis ✔Correct Answer-1. Vessel spasm
2. Formation of the platelet plug
3. Blood coagulation or development of insoluble fibrin clot
4. Clot retraction
5. Clot dissolution
Vessel spasm ✔Correct Answer-MOI: Local and humoral mechanisms
Transiet (<1min)
Vascular smooth muscle contracts to decrease blood flow
local neural reflexes and humoral factors (TXA2) form platelets and contribute to vasoconstriction
Platelet plug formation ✔Correct Answer-vWF (from endothelium) causes adhesion of platelets to
exposed collagen of vessel wall
platelets become activated and release ADP and TXA which cause platelet aggregation and the
formation of a plug
What is the affect of aspirin in plug formation ✔Correct Answer-Aspirin acts as a platelet
aggregation inhibitor
blood coagulation (clotting) ✔Correct Answer-insoluble fibrin threads hold the clot together
anticoagulants such as heparin (mast cells) act to prevent excessive fibrin formation
Clot retraction ✔Correct Answer-Occurs within 20-60min
Actin an myosin in the platelets contract to squeeze serum from the clot and join the edges of the
broken vessel
,If a clot fails to form, what is this indicative of? ✔Correct Answer-Low platelet count
Clot dissolution ✔Correct Answer-Fibrinolysis: Allows blood flow to be re-established and tissue
repair to take place; stands of the clot are dissolved
Plasminogen activators such as tPA and uPA cause the formation of plasmin, which digests fibrin
strands of the clot
What is hypercoagulability? ✔Correct Answer-Conditions that predispose to thrombosis and blood
vessel occlusion
What two things increase in hyper-coagulability states ✔Correct Answer-1. increase in platelet
function
- Increase platelet #
- blod flow disturbance
- Endothelial damage
- platelet aggregation
- all caused by atherosclerosis
2. increase clotting activity
- increase pro coagulation factors
- decrease anticoagulation factors
- inherited or acquired
Types of bleeding disorders ✔Correct Answer-Platelet disorders
- Decrease platelet levels (thrombocytopenia)
- Decrease production in bone marrow
- Increase destruction due to antiplatelet Abs
- Platelets used up forming excessive clots
Coagulation disorders
- Inherited: vWF disease or hemophilia A
- Acquired: liver disease or vitamin k deficiency
What affect do aspirin and NSAIDS have ✔Correct Answer-Inhibit COX 1 and 2 which are involved
in the production of thromboxane and prostaglandins
What shape is RBC ✔Correct Answer-Biconcave for increase SA for O2 diffusion
What is HbA ✔Correct Answer-Adult hemoglobin
What is HbF ✔Correct Answer-fetal hemoglobin
Does HbA or HbF have a higher affinity for O2? ✔Correct Answer-HbF
How many molecules of oxygen can be carried by one molecule of hemoglobin ✔Correct Answer-
four
Hb synthesis and iron cycle ✔Correct Answer-Iron in the hemoglobin department is recycled.
When RBCs age and are destroyed in the spleen, the iron from their hemoglobin is released into the
circulation and returned to bone marrow for incorporation into new red blood cells or to the liver
and other tissue for storage. Iron that is absorbed and not lost in feces, enters the circulation and
immediately combines with B-globulin, apo transferrin, to form transferrin which transports it to the
, plasma. From the plasma, iron can be deposited into tissue cells such as the liver, where it is stored
as ferritin.
Where is majority of iron and it is in the form of what ✔Correct Answer-65% in the form of
hemoglobin
What percent of iron is stored ✔Correct Answer-15-30% stored for later use
Where is iron stored ✔Correct Answer-mainly in the liver
What is the RBC lifespan ✔Correct Answer-Approximately 120 days
Explain the destruction of RBCs ✔Correct Answer-Facilitated by a group of large phagocytic
macrophages found in the spleen, liver, bone marrow, and lymph nodes. These phagocytes recognize
old and defective red cells and ingest and destroy them in a series of enzymatic reactions.
Erythropoiesis ✔Correct Answer-Refers to the production of red blood cells. Erythropoietin
produced by the kidneys acts primarily in later stages of erythropoiesis to stimulate the production
of proerythroblasts from stem cells.
What are proerythroblasts ✔Correct Answer-Formed continuously from pluripotent stem cells in
the bone marrow. They move through a series of divisions each producing a smaller cell as they
continue to develop into mature RBCs
Polycythemia ✔Correct Answer-A disorder characterized by an abnormal increase in RBC count
and hematocrit levels >50%.
Primary: Neoplastic
Secondary: chronically increase EPO
Relative polycythemia ✔Correct Answer-Result of dehydration
Fluid loss results in relative increases of red cell counts and Hgb and Hct values
What is anemia ✔Correct Answer-Abnormally low circulating RBCs or Hb or both
Diminished oxygen carrying capacity
Blood loss anemia ✔Correct Answer-Severity is related to rate of blood loss
Rapid may lead to circulatory collapse (hypovolemia) and death
Slower, chronic blood loss is often reversible and may be asymptomatic until [Hb] < 8g/dL and Fe
deficiency anemia occurs
GIT bleeding
Menstrual disorders
Hemolytic anemia ✔Correct Answer-Reduction in RBCs due to premature RBC destruction
occurring in blood.
4 types of hemolytic anemias ✔Correct Answer-1. Membrane disorders: Hereditary spherocytosis
2. Hemoglobinopathies: Sickle cell disease (HbS gene) or thalassemias
3. Inherited enzyme effect
4. Acquired hemolytic factors