ESSAY Questions Unit 3 – Flashcards

Intrinsic Pathway: Chemical signals within plasma. 1.The Hageman factor is activated by collagen in the blood. 2. Active Hageman factor activates factor XI. 3. Factor XI activates factor IX (xmas factor). 4. Factor IX activates the enzyme factor X. 5. Active factor X converts prothrombin (factor II) to thrombin. Requires Calcium. 6. Thrombin converts fibrinogen (factor I) to fibrin. 7. Thrombin also activates fibrin stabilizing factor or factor XIII (cross links proteins). Extrinsic Pathway: Chemical signals outside plasma. 1. Tissue factor (factor III) comes from damaged tissue. 2. Tissue factor acts as a cofactor and activates factor XII. 3. The VII complex activates factor X. Fibrinolysis: -A damaged vessel wall will start to repair itself, making the clot disintegrate. The enzyme plasmin will help break this down. -The inactive plasminogen will become plasmin. -The molecule prekallikrein helps this activation which must be activated into kallikrein using the Hageman factor. -tPA (tissue plasminogen activator) converts plasminogen into plasmin.

Erythropoiesis: RBC production that is controlled by the glycoprotein erythropoietin (EPO) made by kidneys. Hypoxia (low oxygen in body) is the stimulus used for synthesis and secretion of RBCs. Hypoxia triggers production of a transcriptional factor HIF-1 (hypoxia inducible factor 1). Increased EPO=Increased RBC production. Leukopoiesis: regulated by colony stimulating factors. CSF's are made by endothelial cells, can grow on WBCs, and induce the production of WBCs. G-CSF makes neutrophils and GM-CSFs make monocytes and give rise to macrophages. WBCs make their own chemical signals to communicate affecting production. Differential WBC counts help diagnose diseases: bacterial infections increase WBC count, viral infections increase lymphocyte count, and parasitic worm infections increase eosinophil count. Thrombopoiesis: regulates platelet production and is triggered by the hormone TPO. TPO is a glycoprotein produced by the liver, triggers production of platelets, and comes from the megakaryocyte.

1. Atrial and ventricular diastole (heart at rest): not contracting, pressure in heart is essentially zero and will fill with blood. 2. Atrial systole: most blood enters the ventricles during diastole. When atrial systole occurs it pushes about 20-30% of blood into ventricles. This event follows the P wave on the ECG. 3. Isovolumetric Ventricular Contraction: the depolarization wave of the conduction cells flows down the AV bundle until it reaches the Purkinje fibers resulting in ventricular systole. •Ventricular systole slowly begins and causes the AV valves to close as the pressure increases in the system •Closure of the AV valves represent the first heart sound (S1: lub) •This event follows the QRS on ECG •Ventricular pressure is rising, but is still less than the pressure in the pulmonary trunk and aorta, valves are still closed. •The volume in the ventricles is the EDV, not changing until eject blood. 4. Ventricular Ejection (the heart pumps): pressure in the ventricles is above the aorta/pulmonary truck •The semilunar valves blow open and blood enters arteries •High pressure blood forces low pressure blood through system •The AV valves remain closed so blood doesn't go into atria. •The volume of blood pumped is the stoke volume. 5. Isovolumetric Ventricular Relaxation (2nd heart sound): valves close. •The T wave on ECG repolarization, ventricles relax. •Ventricular pressure begins to drop below the pressure in the arteries. Prevents backflow. •The backflow is prevented by the closure of the semilunar valves and creates the second heart sound (S2) = dup. •Once the semilunar valves are closed the ventricle is a sealed chamber again, isovolumetric relaxation, valves closed.

Hemoglobin synthesis requires adequate iron from diet. 1. Iron is ingested from the diet (animal products, vitamins, spinach, etc.) 2. Iron is absorbed in the small intestine. 3. Iron is transported through transferrin, how iron moves in our bloodstream. 4. Bone marrow takes up iron and uses it to make heme of hemoglobin. 5. RBCs live about 100-120 days in the blood, fragile over time, no organelles or machinery to maintain themselves. 6. Macrophages in the spleen, liver, and bone marrow eat RBCs and recycle them. 7. Amino acids from the globin are recycled for protein synthesis, iron can be recycled to the liver and returned to the bone marrow, and the heme group is converted to bilirubin. 8. Bilirubin and metabolites are excreted in urine (kidneys) or bile, as well as fecal matter (intestines). 9. Iron that has been ingested in greater amounts than needed can be stored in liver and used later (excess iron). Clinical: Hemochromatosis (iron overload) is due to excess iron in the body and is toxic. Initial symptoms include cramping, irritation of GI tract, bloating, internal bleeding, overall corrosion of digestive system. Clinical: Jaundice, yellowing of the skin, occurs when bilirubin in the skin becomes elevated. Too much breakdown of RBCs, can't get rid of fast enough in the bile. Bilirubin is not being eliminated in fecal matter or urine.